Artykuły w czasopismach na temat „Myocardial hypertrophy”
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Tang, Xin, Lihong Pan, Shuang Zhao, Feiyue Dai, Menglin Chao, Hong Jiang, Xuesong Li i in. "SNO-MLP (S-Nitrosylation of Muscle LIM Protein) Facilitates Myocardial Hypertrophy Through TLR3 (Toll-Like Receptor 3)–Mediated RIP3 (Receptor-Interacting Protein Kinase 3) and NLRP3 (NOD-Like Receptor Pyrin Domain Containing 3) Inflammasome Activation". Circulation 141, nr 12 (24.03.2020): 984–1000. http://dx.doi.org/10.1161/circulationaha.119.042336.
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Background: S-nitrosylation (SNO), a prototypic redox-based posttranslational modification, is involved in the pathogenesis of cardiovascular disease. The aim of this study was to determine the role of SNO of MLP (muscle LIM protein) in myocardial hypertrophy, as well as the mechanism by which SNO-MLP modulates hypertrophic growth in response to pressure overload. Methods: Myocardial samples from patients and animal models exhibiting myocardial hypertrophy were examined for SNO-MLP level using biotin-switch methods. SNO sites were further identified through liquid chromatography–tandem mass spectrometry. Denitrosylation of MLP by the mutation of nitrosylation sites or overexpression of S-nitrosoglutathione reductase was used to analyze the contribution of SNO-MLP in myocardial hypertrophy. Downstream effectors of SNO-MLP were screened through mass spectrometry and confirmed by coimmunoprecipitation. Recruitment of TLR3 (Toll-like receptor 3) by SNO-MLP in myocardial hypertrophy was examined in TLR3 small interfering RNA–transfected neonatal rat cardiomyocytes and in a TLR3 knockout mouse model. Results: SNO-MLP level was significantly higher in hypertrophic myocardium from patients and in spontaneously hypertensive rats and mice subjected to transverse aortic constriction. The level of SNO-MLP also increased in angiotensin II– or phenylephrine-treated neonatal rat cardiomyocytes. S-nitrosylated site of MLP at cysteine 79 was identified by liquid chromatography–tandem mass spectrometry and confirmed in neonatal rat cardiomyocytes. Mutation of cysteine 79 significantly reduced hypertrophic growth in angiotensin II– or phenylephrine-treated neonatal rat cardiomyocytes and transverse aortic constriction mice. Reducing SNO-MLP level by overexpression of S-nitrosoglutathione reductase greatly attenuated myocardial hypertrophy. Mechanistically, SNO-MLP stimulated TLR3 binding to MLP in response to hypertrophic stimuli, and disrupted this interaction by downregulating TLR3-attenuated myocardial hypertrophy. SNO-MLP also increased the complex formation between TLR3 and RIP3 (receptor-interacting protein kinase 3). This interaction in turn induced NLRP3 (nucleotide-binding oligomerization domain–like receptor pyrin domain containing 3) inflammasome activation, thereby promoting the development of myocardial hypertrophy. Conclusions: Our findings revealed a key role of SNO-MLP in myocardial hypertrophy and demonstrated TLR3-mediated RIP3 and NLRP3 inflammasome activation as the downstream signaling pathway, which may represent a therapeutic target for myocardial hypertrophy and heart failure.
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Xue, Honghong, Hongtao Shi, Fan Zhang, Hao Li, Chao Li i Qinghua Han. "RIP3 Contributes to Cardiac Hypertrophy by Influencing MLKL-Mediated Calcium Influx". Oxidative Medicine and Cellular Longevity 2022 (14.04.2022): 1–15. http://dx.doi.org/10.1155/2022/5490553.
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Receptor-interacting protein 3(RIP3), a RIP family member, has been reported as a critical regulator of necroptosis and involves in the pathogenesis of various heart diseases. However, its role in the development of myocardial hypertrophy after pressure overload is unclear. We aimed to investigate the roles of RIP3 in pathological cardiac hypertrophy. A rat model of myocardial hypertrophy induced by the aortic banding method was used in this study. Neonatal rat cardiomyocytes (NRCMs) were stimulated with angiotensin II (Ang-II) or phenylephrine (PE) to induce neurohumoral stress. Our results showed that RIP3 level was significantly elevated in the hypertrophic myocardium tissues from patients, rats subjected to AB surgery, and NRCMs treated with Ang-II or PE. After downregulation of RIP3 expression in NRCMs, the phenotypes of myocardial hypertrophy were obviously alleviated. In mechanism, we demonstrated that RIP3 interacts with mixed lineage kinase domain-like protein (MLKL) and promotes its cell membrane localization to increase the influx of calcium within cells, thereby mediating the development of myocardial hypertrophy. More interestingly, we found the blockage of calcium influx by 2-aminoethoxydiphenyl borate, and lanthanum chloride efficiently reverses RIP3-induced cardiac remodeling in NRCMs. Taken together, our findings indicate a key role of the RIP3-MLKL signaling pathway in myocardial hypertrophy, which may be a novel promising treatment strategy for myocardial hypertrophy.
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Parker, Thomas G., i James N. Tsoporis. "Induction of S100β in Myocardium: An Intrinsic Inhibitor of Cardiac Hypertrophy". Canadian Journal of Applied Physiology 23, nr 4 (1.08.1998): 377–89. http://dx.doi.org/10.1139/h98-022.
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Cardiac hypertrophy induced by pressure overload and following myocardial infarction entails regulation of myocardial gene expression, recapitulating an embryonic phenotype, including activation of fetal β-myosin heavy chain and skeletal α-actin. Progressive hypertrophy and alterations in gene expression may contribute to myocardial failure. Although signaling pathways that contribute to hypertrophy development have been identified, intrinsic cardiac regulators that limit hypertrophic response have not been determined. The β subunit of S100 protein is induced in the myocardium of human subjects and an experimental rat model following myocardial infarction. Forced S100β expression in neonatal rat cardiac myocyte cultures and high level expression of S100β in transgenic mice hearts inhibit cardiac hypertrophy and the associated phenotype by modulating protein kinase C-dependent pathways. S100β expression is probably a component of the myocyte response to trophic stimulation that serves as a negative feedback mechanism to limit cellular growth and the associated alterations in gene expression. Key words: gene expression, cardiac myocytes, growth factors, heart failure, calcium-binding proteins
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Tasnic, Mihail, Valeriu Revenco i Ilia Catereniuc. "Correlations of myocardial bridges with left ventricle myocardial hypertrophy and prepontin coronary atherosclerosis". Moldovan Medical Journal 64, nr 5 (grudzień 2021): 21–26. http://dx.doi.org/10.52418/moldovan-med-j.64-5.21.04.
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Background: Of particular interest are the studies researching the correlations of myocardial bridges with hypertrophic cardiomyopathy and correlations of thick myocardial bridges with the development of coronary atherosclerosis in the proximal to the bridge arterial part. Material and methods: Assessment of the correlation between myocardial bridges, coronary atherosclerosis, and the degree of hypertrophy of the left ventricle was performed by retrospective analysis of 6168 coronary angiography protocols (2012-2019) and echocardiographic data from patients’ clinical records. Results: Moderate systolic compression predominated, and the number of patients detected with severe under the bridge systolic coronary stenosis was double as in patients with nonsignificant coronary atherosclerosis. From the total number, patients with myocardial hypertrophy and myocardial bridges were twice less when compared with the patients with the normal myocardial thickness. The comparative research did not show any interdependence between the degree of vascular compression and the degree of left ventricular myocardial hypertrophy. Proximal to the bridges atherosclerosis was detected in 32% of cases without correlation with the force of the myocardial bridge. Conclusions: The study showed the absence of the correlation between the degree of arterial stenosis caused by the bridge and the degree of hypertrophy of the ventricular myocardium as well as the degree of proximal to the bridge atherosclerosis. Important finding was that the degree of coronary systolic compression is higher in patients with moderate and severe proximal to the bridge atherosclerosis.
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Ouattara, Alexandre, Olivier Langeron, Rachid Souktani, Stéphane Mouren, Pierre Coriat i Bruno Riou. "Myocardial and Coronary Effects of Propofol in Rabbits with Compensated Cardiac Hypertrophy". Anesthesiology 95, nr 3 (1.09.2001): 699–707. http://dx.doi.org/10.1097/00000542-200109000-00024.
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Background Myocardial effects of propofol have been previously investigated but most studies have been performed in healthy hearts. This study compared the cardiac effects of propofol on isolated normal and hypertrophic rabbits hearts. Methods The effects of propofol (10-1,000 microM) on myocardial contractility, relaxation, coronary flow and oxygen consumption were investigated in hearts from rabbits with pressure overload-induced left ventricular hypertrophy (LVH group, n = 20) after aortic abdominal banding and from sham-operated control rabbits (SHAM group, n = 10), using an isolated and erythrocyte-perfused heart model. In addition, to assess the myocardial and coronary effects of propofol in more severe LVH, hearts with a degree of hypertrophy greater than 140% were selected (severe LVH group, n = 7). Results The cardiac hypertrophy model induced significant left ventricular hypertrophy (136+/-21%, P < 0.05). The pressure-volume relation showed normal systolic function but an altered diastolic compliance in hypertrophic hearts. Propofol only decreased myocardial contractility and relaxation at supratherapeutic concentrations (> or = 300 microM) in SHAM and LVH groups. The decrease in myocardial performances was not significantly different in SHAM and LVH groups. Propofol induced a significant increase in coronary blood flow which was not significantly different between groups. In severe LVH group, the degree of hypertrophy reached to 157+/-23%. Similarly, the effects of concentrations of propofol were not significantly different from the SHAM group. Conclusions Propofol only decreased myocardial function at supratherapeutic concentrations. The myocardial and coronary effects of propofol were not significantly modified in cardiac hypertrophy.
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Lu, Dan, Jizheng Wang, Jing Li, Feifei Guan, Xu Zhang, Wei Dong, Ning Liu, Shan Gao i Lianfeng Zhang. "Meox1 accelerates myocardial hypertrophic decompensation through Gata4". Cardiovascular Research 114, nr 2 (16.11.2017): 300–311. http://dx.doi.org/10.1093/cvr/cvx222.
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AbstractAimsPathological hypertrophy is the result of gene network regulation, which ultimately leads to adverse cardiac remodelling and heart failure (HF) and is accompanied by the reactivation of a ‘foetal gene programme’. The Mesenchyme homeobox 1 (Meox1) gene is one of the foetal programme genes. Meox1 may play a role in embryonic development, but its regulation of pathological hypertrophy is not known. Therefore, this study investigated the effect of Meox1 on pathological hypertrophy, including familial and pressure overload-induced hypertrophy, and its potential mechanism of action.Methods and resultsMeox1 expression was markedly down-regulated in the wild-type adult mouse heart with age, and expression was up-regulated in heart tissues from familial dilated cardiomyopathy (FDCM) mice of the cTnTR141W strain, familial hypertrophic cardiomyopathy (FHCM) mice of the cTnTR92Q strain, pressure overload-induced HF mice, and hypertrophic cardiomyopathy (HCM) patients. Echocardiography, histopathology, and hypertrophic molecular markers consistently demonstrated that Meox1 overexpression exacerbated the phenotypes in FHCM and in mice with thoracic aorta constriction (TAC), and that Meox1 knockdown improved the pathological changes. Gata4 was identified as a potential downstream target of Meox1 using digital gene expression (DGE) profiling, real-time PCR, and bioinformatics analysis. Promoter activity data and chromatin immunoprecipitation (ChIP) and Gata4 knockdown analyses indicated that Meox1 acted via activation of Gata4 transcription.ConclusionMeox1 accelerated decompensation via the downstream target Gata4, at least in part directly. Meox1 and other foetal programme genes form a highly interconnected network, which offers multiple therapeutic entry points to dampen the aberrant expression of foetal genes and pathological hypertrophy.
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Chiu, Chiung-Zuan, Bao-Wei Wang, Tun-Hui Chung i Kou-Gi Shyu. "Angiotensin II and the ERK pathway mediate the induction of myocardin by hypoxia in cultured rat neonatal cardiomyocytes". Clinical Science 119, nr 7 (22.06.2010): 273–82. http://dx.doi.org/10.1042/cs20100084.
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Hypoxic injury to cardiomyocytes is a stress that causes cardiac pathology through cardiac-restricted gene expression. SRF (serum-response factor) and myocardin are important for cardiomyocyte growth and differentiation in response to myocardial injuries. Previous studies have indicated that AngII (angiotensin II) stimulates both myocardin expression and cardiomyocyte hypertrophy. In the present study, we evaluated the expression of myocardin and AngII after hypoxia in regulating gene transcription in neonatal cardiomyocytes. Cultured rat neonatal cardiomyocytes were subjected to hypoxia, and the expression of myocardin and AngII were evaluated. Different signal transduction pathway inhibitors were used to identify the pathway(s) responsible for myocardin expression. An EMSA (electrophoretic mobility-shift assay) was used to identify myocardin/SRF binding, and a luciferase assay was used to identify transcriptional activity of myocardin/SRF in neonatal cardiomyocytes. Both myocardin and AngII expression increased after hypoxia, with AngII appearing at an earlier time point than myocardin. Myocardin expression was stimulated by AngII and ERK (extracellular-signal-regulated kinase) phosphorylation, but was suppressed by an ARB (AngII type 1 receptor blocker), an ERK pathway inhibitor and myocardin siRNA (small interfering RNA). AngII increased both myocardin expression and transcription in neonatal cardiomyocytes. Binding of myocardin/SRF was identified using an EMSA, and a luciferase assay indicated the transcription of myocardin/SRF in neonatal cardiomyocytes. Increased BNP (B-type natriuretic peptide), MHC (myosin heavy chain) and [3H]proline incorporation into cardiomyocytes was identified after hypoxia with the presence of myocardin in hypertrophic cardiomyocytes. In conclusion, hypoxia in cardiomyocytes increased myocardin expression, which is mediated by the induction of AngII and the ERK pathway, to cause cardiomyocyte hypertrophy. Myocardial hypertrophy was identified as an increase in transcriptional activities, elevated hypertrophic and cardiomyocyte phenotype markers, and morphological hypertrophic changes in cardiomyocytes.
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Liu, Xiuhua, Tianbo Li, Sheng Sun, Feifei Xu i Yiguang Wang. "Role of myofibrillogenesis regulator-1 in myocardial hypertrophy". American Journal of Physiology-Heart and Circulatory Physiology 290, nr 1 (styczeń 2006): H279—H285. http://dx.doi.org/10.1152/ajpheart.00247.2005.
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Myofibrillogenesis regulator-1 (MR-1) is a novel homologous gene, identified from a human skeletal muscle cDNA library, that interacts with contractile proteins and exists in human myocardial myofibrils. The present study investigated MR-1 protein expression in hypertrophied myocardium and MR-1 involvement in cardiac hypertrophy. Cardiac hypertrophy was induced by abdominal aortic stenosis (AAS) in Sprague-Dawley rats. Left ventricular (LV) hypertrophy was assessed by the ratio of LV wet weight to whole heart weight (LV/HW) or LV weight to body weight (LV/BW). Rat MR-1 (rMR-1) expression in the myocardium was detected by immunohistochemical and Western blotting analysis. Hypertrophy was induced by ANG II incubation in cultured neonatal rat cardiomyocytes. The effect of rMR-1 RNA interference on ANG II-induced hypertrophy was studied by transfection of cardiomyocytes with an RNA interference plasmid, pSi-1, which targets rMR-1. Hypertrophy in cardiomyocytes was assessed by [3H]Leu incorporation and myocyte size. rMR-1 protein expression in cardiomyocytes was detected by Western blotting. We found that AAS resulted in a significant increase in LV/HW and LV/BW: 89% and 86%, respectively ( P < 0.01). Immunohistochemistry and Western blot analysis demonstrated upregulated rMR-1 protein expression in hypertrophic myocardium. ANG II induced a 24% increase in [3H]Leu incorporation and a 65.8% increase in cell size compared with control cardiomyocytes ( P < 0.01), which was prevented by treatment with losartan, an angiotensin (AT1) receptor inhibitor, or transfection with pSi-1. rMR-1 expression increased in ANG II-induced hypertrophied cardiomyocytes, and pSi-1 transfection abolished the upregulation. These findings suggest that MR-1 is associated with cardiac hypertrophy in rats in vivo and in vitro.
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Lv, Shichao, Qiang Wang, Meifang Wu, Meng Li, Xiaojing Wang, Ling Xu i Junping Zhang. "QiShenYiQi Pill Improves Myocardial Hypertrophy Caused by Pressure Overload in Rats". Evidence-Based Complementary and Alternative Medicine 2021 (16.06.2021): 1–10. http://dx.doi.org/10.1155/2021/5536723.
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Pressure-overloaded myocardial hypertrophy is an independent risk factor for various cardiovascular diseases (CVDs), such as heart failure (HF), arrhythmia, and even sudden death. It is reported that QiShenYiQi pill (QSYQ) is widely used in the treatment of CVDs and can prevent pathological hypertrophy of myocardium, but its specific mechanism is still unclear. In this study, a rat model of myocardial hypertrophy was established through the pressure overload caused by abdominal aortic constriction in Wistar rats. The rats were randomly divided into model group, valsartan group, and QSYQ group, and sham-operated animals served as the control group. At the 4 and 8 weeks of intervention, the general morphology of the heart, myocardial collagen content, collagen volume factor (CVF), collagen type I, collagen type III, myocardial pathological changes, and the expression of ANP, β-MHC, TGF-β1, and CTGF were analyzed, respectively, in order to explore the possible effect of QSYQ on the mechanism of myocardial hypertrophy. We observed that QSYQ could effectively improve myocardial hypertrophy in pressure-overloaded rats, which was related to the regulatory mechanism of TGF-β1 and CTGF.
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Zheng, Xi, Fuxiang Su, Ze Kang, Jingyuan Li, Chenyang Zhang, Yujia Zhang i Liying Hao. "Analysis of Therapeutic Targets of A Novel Peptide Athycaltide-1 in the Treatment of Isoproterenol-Induced Pathological Myocardial Hypertrophy". Cardiovascular Therapeutics 2022 (2.05.2022): 1–13. http://dx.doi.org/10.1155/2022/2715084.
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Myocardial hypertrophy is a pathological feature of many heart diseases. This is a complex process involving all types of cells in the heart and interactions with circulating cells. This study is aimed at identifying the differentially expressed proteins (DEPs) in myocardial hypertrophy rats induced by isoprenaline (ISO) and treated with novel peptide Athycaltide-1 (ATH-1) and exploring the mechanism of its improvement. ITRAQ was performed to compare the three different heart states in control group, ISO group, and ATH-1 group. Pairwise comparison showed that there were 121 DEPs in ISO/control (96 upregulated and 25 downregulated), 47 DEPs in ATH-1/ISO (27 upregulated and 20 downregulated), and 116 DEPs in ATH-1/control (77 upregulated and 39 downregulated). Protein network analysis was then performed using the STRING software. Functional analysis revealed that Hspa1 protein, oxidative stress, and MAPK signaling pathway were significantly involved in the occurrence and development of myocardial hypertrophy, which was further validated by vivo model. It is proved that ATH-1 can reduce the expression of Hspa1 protein and the level of oxidative stress in hypertrophic myocardium and further inhibit the phosphorylation of p38 MAPK, JNK, and ERK1/2.
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Liu, Yao-Lung, Chiu-Ching Huang, Chiz-Chung Chang, Che-Yi Chou, Shih-Yi Lin, I.-Kuan Wang, Dennis Jine-Yuan Hsieh, Gwo-Ping Jong, Chih-Yang Huang i Chao-Min Wang. "Hyperphosphate-Induced Myocardial Hypertrophy through the GATA-4/NFAT-3 Signaling Pathway Is Attenuated by ERK Inhibitor Treatment". Cardiorenal Medicine 5, nr 2 (2015): 79–88. http://dx.doi.org/10.1159/000371454.
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Background/Aims: Numerous epidemiological studies have associated elevated serum phosphorus levels with cardiovascular disease and the risk of death in the general population as well as in chronic kidney disease (CKD) and dialysis patients. In this study, we explored whether elevated phosphate conditions induce cardiac hypertrophy and attempted to identify the molecular and cellular mechanisms in the hypertrophic response. Methods: H9c2 myocardial cells were incubated in high-phosphate conditions to induce hypertrophy. Pathological hypertrophic responses were measured in terms of cell size, arrangement of actin filaments, and hypertrophy markers such as atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in myocardial cells. Several transcriptional factors involved in cardiac hypertrophy development were measured to investigate the molecular pathways involved in elevated phosphate-induced cardiac hypertrophy. Results: High-phosphate conditions induced cellular hypertrophy, marked by increased cell size, reorganization of actin filaments, and upregulation of both ANP and BNP in H9c2 cells. Both upstream calcineurin and downstream transcription factors, including GATA-4 and NFAT-3, were significantly increased under hyperphosphate conditions. Moreover, both MEK1/2 and ERK1/2 expression increased significantly, and cellular hypertrophy was markedly attenuated by U0126, an ERK1/2 inhibitor. Conclusions: These results suggest that hyperphosphate conditions induce myocardial hypertrophy through the ERK signaling pathway in H9c2 cells. Our findings provide a link between the hyperphosphate-induced response and the ERK/NFAT-3 signaling pathway that mediates the development of cardiac hypertrophy. In view of the potent and selective activity of the ERK inhibitor U0126, this agent warrants further investigation as a candidate for preventing hyperphosphate-induced cardiac hypertrophy in CKD and dialysis patients.
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Nakamura, Teruya, Kunio Matsumoto, Shinya Mizuno, Yoshiki Sawa, Hikaru Matsuda i Toshikazu Nakamura. "Hepatocyte growth factor prevents tissue fibrosis, remodeling, and dysfunction in cardiomyopathic hamster hearts". American Journal of Physiology-Heart and Circulatory Physiology 288, nr 5 (maj 2005): H2131—H2139. http://dx.doi.org/10.1152/ajpheart.01239.2003.
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Structural remodeling of the myocardium, including myocyte hypertrophy, myocardial fibrosis, and dilatation, drives functional impairment in various forms of acquired and hereditary cardiomyopathy. Using cardiomyopathic Syrian hamsters with a genetic defect in δ-sarcoglycan, we investigated the potential involvement of hepatocyte growth factor (HGF) in the pathophysiology and therapeutics related to dilated cardiomyopathy, because HGF has previously been shown to be cytoprotective and to have benefits in acute heart injury. Late-stage TO-2 cardiomyopathic hamsters showed severe cardiac dysfunction and fibrosis, accompanied by increases in myocardial expression of transforming growth factor-β1 (TGF-β1), a growth factor responsible for tissue fibrosis. Conversely, HGF was downregulated in late-stage myopathic hearts. Treatment with recombinant human HGF for 3 wk suppressed cardiac fibrosis, accompanied by a decreased expression of TGF-β1 and type I collagen. Suppression of TGF-β1 and type I collagen by HGF was also shown in cultured cardiac myofibroblasts. Likewise, HGF suppressed myocardial hypertrophy, apoptosis in cardiomyocytes, and expression of atrial natriuretic polypeptide, a molecular marker of hypertrophy. Importantly, downregulation of the fibrogenic and hypertrophic genes by HGF treatment was associated with improved cardiac function. Thus the decrease in endogenous HGF levels may participate in the susceptibility of cardiac tissue to hypertrophy and fibrosis, and exogenous HGF led to therapeutic benefits in case of dilated cardiomyopathy in this model, even at the late-stage treatment.
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Koga, Kiyokazu, Agnes Kenessey i Kaie Ojamaa. "Macrophage migration inhibitory factor antagonizes pressure overload-induced cardiac hypertrophy". American Journal of Physiology-Heart and Circulatory Physiology 304, nr 2 (15.01.2013): H282—H293. http://dx.doi.org/10.1152/ajpheart.00595.2012.
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Macrophage migration inhibitory factor (MIF) functions as a proinflammatory cytokine when secreted from the cell, but it also exhibits antioxidant properties by virtue of its intrinsic oxidoreductase activity. Since increased production of ROS is implicated in the development of left ventricular hypertrophy, we hypothesized that the redox activity of MIF protects the myocardium when exposed to hemodynamic stress. In a mouse model of myocardial hypertrophy induced by transverse aortic coarctation (TAC) for 10 days, we showed that growth of the MIF-deficient heart was significantly greater by 32% compared with wild-type (WT) TAC hearts and that fibrosis was increased by fourfold (2.62 ± 0.2% vs. 0.6 ± 0.1%). Circulating MIF was increased in TAC animals, and expression of MIF receptor, CD74, was increased in the hypertrophic myocardium. Gene expression analysis showed a 10-fold increase ( P < 0.01) in ROS-generating mitochondrial NADPH oxidase and 2- to 3-fold reductions ( P < 0.01) in mitochondrial SOD2 and mitochondrial aconitase activities, indicating enhanced oxidative injury in the hypertrophied MIF-deficient ventricle. Hypertrophic signaling pathways showed that phosphorylation of cytosolic glycogen synthase kinase-3α was greater ( P < 0.05) at baseline in MIF-deficient hearts than in WT hearts and remained elevated after 10-day TAC. In the hemodynamically stressed MIF-deficient heart, nuclear p21CIP1 increased sevenfold ( P < 0.01), and the cytosolic increase of phospho-p21CIP1 was significantly greater than in WT TAC hearts. We conclude that MIF antagonizes myocardial hypertrophy and fibrosis in response to hemodynamic stress by maintaining a redox homeostatic phenotype and attenuating stress-induced activation of hypertrophic signaling pathways.
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Leontyeva, I. V., N. V. Shcherbakova, E. P. Kalachanova, S. A. Thermosesov i V. S. Sukhorukov. "Hypertrophic cardiomyopathy caused by mutations in the <I>PRKAG2</I> gene". Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 67, nr 4 (21.09.2022): 99–107. http://dx.doi.org/10.21508/1027-4065-2022-67-4-99-107.
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Clinical observations of three cases of hypertrophic cardiomyopathy caused by mutations in the PRKAG2 gene with a debut in early childhood are presented. The sisters whose father suffered from a severe form of hypertrophic cardiomyopathy in combination with Wolf—Parkinson—White syndrome and died at a young age from progressive heart failure are described. Early manifestation of the disease is characteristic, while there was a combination of ventricular preexitation syndrome and myocardial hypertrophy with rapid progression to extreme values. Hypertrophy was concentric symmetrical and biventricular. The main clinical symptom in the first observation was frequent paroxysms of supraventricular tachycardia. New atrioventricular fenestrations were detected during dynamic observation, insufficient effectiveness of radiofrequency ablation, recurrence of supraventricular tachycardia, and a good response to propafenone were noted. The third clinical case is sporadic, a long-term follow-up for 15 years is presented and clearly reflects the progression of the increase in myocardial hypertrophy and cardiac arrhythmias. The disease debuted from an early age in the form of hypertrophy in combination with severe bradycardia, which made drug therapy difficult. Due to the high risk of sudden cardiac death against the background of extreme myocardial hypertrophy, a cardioverter defibrillator was implanted. Signs of mitochondrial insufficiency according to skeletal muscle biopsy are described.
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Ji, Xiao-Bing, Xiu-Rong Li, Hao-Ding, Qi Sun, Yang Zhou, Ping Wen, Chun-Sun Dai i Jun-Wei Yang. "Inhibition of Uncoupling Protein 2 Attenuates Cardiac Hypertrophy Induced by Transverse Aortic Constriction in Mice". Cellular Physiology and Biochemistry 36, nr 5 (2015): 1688–98. http://dx.doi.org/10.1159/000430142.
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Background: Uncoupling protein 2 (UCP2) is critical in regulating energy metabolism. Due to the significant change in energy metabolism of myocardium upon pressure overload, we hypothesize that UCP2 could contribute to the etiology of cardiac hypertrophy. Methods: Adult male C57BL/6J mice were subjected to pressure overload by using transverse aortic constriction (TAC), and then received genipin (a UCP2 selective inhibitor; 25 mg/kg/d, ip) or vehicle for three weeks prior to histologic assessment of myocardial hypertrophy. ATP concentration, ROS level, and myocardial apoptosis were also examined. A parallel set of experiments was also conducted in UCP2-/- mice. Results: TAC induced left ventricular hypertrophy, as reflected by increased ventricular weight/thickness and increased size of myocardial cell (vs. sham controls). ATP concentration was decreased; ROS level was increased. Apoptosis and fibrosis markers were increased. TAC increased mitochondrial UCP2 expression in the myocardium at both mRNA and protein levels. Genipin treatment attenuated cardiac hypertrophy and the histologic/biochemical changes described above. Hypertrophy and associated changes induced by TAC in UCP2-/- mice were much less pronounced than in WT mice. Conclusions: Blocking UCP2 expression attenuates cardiac hypertrophy induced by pressure overload.
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Chernykh, N. Yu, A. A. Tarasova, O. S. Groznova i I. M. Shigabeev. "Left ventricular myocardial strain and electrocardiographic changes in children with hypertrophic cardiomyopathy". Meditsinskiy sovet = Medical Council, nr 11 (12.08.2021): 124–32. http://dx.doi.org/10.21518/2079-701x-2021-11-124-132.
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Abstract Introduction. Hypertrophic cardiomyopathy is one of the most common diseases of the myocardium in children. Meanwhile, the relationship between indicators of strain and electrocardiographic changes, their diagnostic significance for children with hypertrophic cardiomyopathy remains an insufficiently well-studied issue.Purpose. Тo analyze the relationship between indicators of strain of the left ventricular and ECG in children with hypertrophic cardiomyopathy (HCM).Materials and methods. Have been examined 61 patients with an asymmetric form of hypertrophic cardiomyopathy aged from 7 to 17 years. Of these, 45 (73.8%) children with nonobstructive form, 16 (26.2%) children with obstructive form. Electrocardiography (ECG) and 24-hour Holter monitoring ECG had performed. The parameters of global longitudinal, radial and circular of the left ventricular myocardial strain and their rates had determined by echocardiography in the 2D speckle tracking modeResults. In children with HCM, ECG signs of hypertrophy were studied (deviation of the electrical axis to the left, the predominance of the R wave in lead I, V6 over the S wave, the predominance of the S wave in lead V1 over the R wave) and myocardial ischemia (inversion of the T wave and a decrease in the ST segment in the leads I, II, V5, V6), rhythm and conduction disorders (ventricular extrasystole, degree I atrioventricular block, expansion of the QRS complex in leads V1-V3, incomplete blockade of the anterior left branch of the His bundle, increased duration of terminal activation), which significantly prevailed in obstructive form versus non-obstructive form. A decrease in the global longitudinal, radial, circular strain of the left ventricular myocardium and their rates had found, which had significantly more pronounced in the group with obstructive HCM. Inverse correlations had found between the parameters of strain and ECG-signs of hypertrophy and myocardial ischemia, conduction disorders, more pronounced between the parameters of longitudinal strain and ECG with a significant predominance in the obstructive form of the disease.Conclusions. In children with obstructive HCM, compared with the non-obstructive form, there have significantly more pronounced signs of myocardial hypertrophy and ischemia, rhythm and conduction disorders on the ECG and with 24-hour Holter monitoring ECG.
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Aluja, David, Sara Delgado-Tomás, Marisol Ruiz-Meana, José A. Barrabés i Javier Inserte. "Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy". International Journal of Molecular Sciences 23, nr 8 (7.04.2022): 4103. http://dx.doi.org/10.3390/ijms23084103.
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Despite advances in its treatment, heart failure remains a major cause of morbidity and mortality, evidencing an urgent need for novel mechanism-based targets and strategies. Myocardial hypertrophy, caused by a wide variety of chronic stress stimuli, represents an independent risk factor for the development of heart failure, and its prevention constitutes a clinical objective. Recent studies performed in preclinical animal models support the contribution of the Ca2+-dependent cysteine proteases calpains in regulating the hypertrophic process and highlight the feasibility of their long-term inhibition as a pharmacological strategy. In this review, we discuss the existing evidence implicating calpains in the development of cardiac hypertrophy, as well as the latest advances in unraveling the underlying mechanisms. Finally, we provide an updated overview of calpain inhibitors that have been explored in preclinical models of cardiac hypertrophy and the progress made in developing new compounds that may serve for testing the efficacy of calpain inhibition in the treatment of pathological cardiac hypertrophy.
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Wang, Hui, Yuqin Zhang, Shuwen Guo, Jiani Wu, Wang’ou Lin, Binyue Zhang, Pengfei Feng i in. "Effects of Yiqi Huoxue Decoction on Post-Myocardial Infarction Cardiac Nerve Remodeling and Cardiomyocyte Hypertrophy in Rats". Evidence-Based Complementary and Alternative Medicine 2021 (21.08.2021): 1–16. http://dx.doi.org/10.1155/2021/5168574.
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Myocardial infarction can lead to ventricular remodeling and arrhythmia, which is closely related to nerve remodeling. Our previous study found that Yiqi Huoxue decoction (YQHX) can improve ventricular remodeling and reduce myocardial damage. Therefore, in this study, we observed the effect of YQHX on cardiac neural remodeling and cardiomyocyte hypertrophy and its possible mechanism. This research is composed of two parts: animal and H9c2 cells experiments. The animal model of acute myocardial infarction was established by ligating the left anterior descending coronary artery in Sprague Dawley (SD) rats. H9c2 cells were placed in 94% N2, 5% CO2, and 1% O2 hypoxic environment for 12 hours to replicate the hypoglycemic hypoxia model. The experimental results showed that, compared with the MI group, YQHX can significantly improve heart function after myocardial infarction and reduce nerve remodeling and myocardial hypertrophy. Pathological structure observation demonstrated reducing myocardial tissue damage and decreasing of cell cross-sectional area, diameter, and circumference. The positive rate of TH declined apparently, and the sympathetic nerve density was lower than that of the MI group. After YQHX was given for 28 days, the proneural remodeling factors TH, NGF, and GAP43 in the marginal zone of infarction and stellate ganglion decreased obviously while the inhibitory nerve remodeling factor Sema-3A increased. The myocardial hypertrophic protein ANP and β-MHC were also significantly inhibited with p-ERK1/2 protein expression level prominently reduced. There was no difference between the YQHX group and the Meto group. After myocardial infarction, nerve remodeling was seen in the marginal area of infarction and stellate ganglion, and the neuropeptides released by which promoted myocardial hypertrophy. The mechanism may be related to the ERK1/2 signaling pathway. YQHX could regulate the ERK1/2 signaling pathway, inhibit the release of nerve remodeling factors and myocardial hypertrophy protein to reduce nerve remodeling, and relieve myocardial hypertrophy.
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Chen, Chao-Yi, Jyh-Gang Leu, Kuan-Yu Lin, Chin-Yu Shih i Yao-Jen Liang. "Serotonin receptor subtype-2B signaling is associated with interleukin-18-induced cardiomyoblast hypertrophy in vitro". Asian Biomedicine 16, nr 2 (1.04.2022): 79–87. http://dx.doi.org/10.2478/abm-2022-0010.
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Abstract Background In patients with heart failure, interleukin-18 (IL-18) levels increase in the circulatory system and injured myocardial tissue. Serotonin (5-hydroxytryptamine) receptors subtype 2B (HTR2B) play an essential role in cardiac function and development, and their overexpression in rats leads to myocardial hypertrophy. Epigallocatechin gallate (EGCG) is cardioprotective in myocardial ischemia–reperfusion injury in rats and can prevent pressure overload-mediated cardiac hypertrophy in vivo. Mice deficient in peroxisome proliferator-activated receptor delta (PPARδ) can have cardiac dysfunction, myocardial hypertrophy, and heart failure. Matrix metalloproteinases (MMPs) are possibly involved in cardiac remodeling. However, the relationship between IL-18 signaling, cardiac hypertrophy, and the molecular mechanisms involved remain to be fully elucidated. Objectives To elucidate the relationship between HTR2B and IL-18-induced myocardial hypertrophy and examine the antihypertrophic effects of EGCG and PPARδ. Methods We induced H9c2 cardiomyoblast hypertrophy with IL-18 in vitro and investigated the downstream signaling by real-time polymerase chain reaction (PCR) and western blotting. Hypertrophy was assessed by flow cytometry. We determined the effects of EGCG and PPARδ on IL-18-induced hypertrophic signaling via HTR2B-dependent mechanisms. Results IL-18-induced H9c2 hypertrophy upregulated brain natriuretic peptide (BNP) protein and mRNA expression by inducing the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and the hypertrophy was attenuated by pretreatment with EGCG (20 μM) and L-165,041 (2 μM), a PPARδ agonist. IL-18 upregulated the expression of HTR2B, which was inhibited by pretreatment with EGCG and L-165,041. SB215505 (0.1 μM), a HTR2B antagonist and siRNA for HTR2B, attenuated H9c2 hypertrophy significantly. Inhibition of HTR2B also downregulated the expression of MMP-3 and MMP-9. Conclusions IL-18 and HTR2B play critical roles in cardiomyoblast hypertrophy. EGCG and L-165,041 inhibit the expression of HTR2B and augment remodeling of H9c2 cardiomyoblasts, possibly mediated by MMP-3 and MMP-9.
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Xia, Huiting, Aqeela Zahra, Meng Jia, Qun Wang, Yunfu Wang, Susan L. Campbell i Jianping Wu. "Na+/H+ Exchanger 1, a Potential Therapeutic Drug Target for Cardiac Hypertrophy and Heart Failure". Pharmaceuticals 15, nr 7 (15.07.2022): 875. http://dx.doi.org/10.3390/ph15070875.
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Cardiac hypertrophy is defined as increased heart mass in response to increased hemodynamic requirements. Long-term cardiac hypertrophy, if not counteracted, will ultimately lead to heart failure. The incidence of heart failure is related to myocardial infarction, which could be salvaged by reperfusion and ultimately invites unfavorable myocardial ischemia-reperfusion injury. The Na+/H+ exchangers (NHEs) are membrane transporters that exchange one intracellular proton for one extracellular Na+. The first discovered NHE isoform, NHE1, is expressed almost ubiquitously in all tissues, especially in the myocardium. During myocardial ischemia-reperfusion, NHE1 catalyzes increased uptake of intracellular Na+, which in turn leads to Ca2+ overload and subsequently myocardial injury. Numerous preclinical research has shown that NHE1 is involved in cardiac hypertrophy and heart failure, but the exact molecular mechanisms remain elusive. The objective of this review is to demonstrate the potential role of NHE1 in cardiac hypertrophy and heart failure and investigate the underlying mechanisms.
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Bishop, Sanford P. "The Myocardial Cell: Normal Growth, Cardiac Hypertrophy and Response to Injury". Toxicologic Pathology 18, nr 4a (styczeń 1990): 438–53. http://dx.doi.org/10.1177/0192623390004part_102.
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Development and growth of cardiac muscle tissue is controlled by a variety of intrinsic and extrinsic factors. Fetal growth is by hyperplasia, is strongly governed by inherent factors and is only slightly modified by external environmental factors. The number of cell divisions is species-dependent and normally stops shortly after birth. Developing blood volume and pressure dictate the hypertrophic stage of normal growth, and this may be further modified by abnormal hemodynamic and humoral factors. Connective tissue, neural and vascular components of the myocardium mature along with the myocyte, and alterations in these structures profoundly affect myocyte function. Hypertrophy beyond normal growth is the response of the myocyte by increased protein synthesis to various stimuli including hemodynamic, humoral and ischemic factors. Injury to normal and hypertrophied myocardium may vary due to structural and metabolic adaptations of hypertrophied tissue, such as connective tissue proliferation, vascular supply alterations and glycolytic metabolic potential. Ischemic effects influence not only cell necrosis, but also hypertrophy and congestive myocardial failure.
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Nakata, Yohei, Muneo Yoshibayashi, Toshiya Yonemura, Shinji Uemoto, Yukihiro Inomata, Koichi Tanaka i Kenshi Furusho. "TACROLIMUS AND MYOCARDIAL HYPERTROPHY". Transplantation 69, nr 9 (maj 2000): 1960–62. http://dx.doi.org/10.1097/00007890-200005150-00039.
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Suzuki, Jun-ichi, Hiroki Sato, Makoto Kaneko, Asuka Yoshida, Norio Aoyama, Shouta Akimoto, Kouji Wakayama i in. "Periodontitis and myocardial hypertrophy". Hypertension Research 40, nr 4 (10.11.2016): 324–28. http://dx.doi.org/10.1038/hr.2016.146.
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Nakagami, Hironori, i James K. Liao. "Statins and myocardial hypertrophy". Coronary Artery Disease 15, nr 5 (sierpień 2004): 247–50. http://dx.doi.org/10.1097/01.mca.0000130229.18685.b9.
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Sugden, Peter H. "Signaling in Myocardial Hypertrophy". Circulation Research 84, nr 6 (2.04.1999): 633–46. http://dx.doi.org/10.1161/01.res.84.6.633.
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Hirsch, Alan T., John A. Opsahl, Mary M. Lunzer i Stephen A. Katz. "Active renin and angiotensinogen in cardiac interstitial fluid after myocardial infarction". American Journal of Physiology-Heart and Circulatory Physiology 276, nr 6 (1.06.1999): H1818—H1826. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1818.
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The renin-angiotensin system promotes cardiac hypertrophy after myocardial infarction. The purpose of this study was to measure renin and angiotensinogen in plasma and myocardium 10 days after myocardial infarction. Infarction involving 45 ± 4% of left ventricular circumference with accompanying hypertrophy was induced in rats ( n = 14). Plasma and myocardial renin were increased after infarction compared with sham controls ( n = 8) (27.4 ± 3.2 vs. 7.5 ± 1.8 ng ANG I ⋅ ml plasma ⋅ h−1, P < 0.0002; and 8.8 ± 1.6 vs. 2.5 ± 0.1 ng ANG I ⋅ g myocardium−1 ⋅ h−1, P < 0.008, respectively). After infarction, myocardial renin was correlated with infarct size ( r = 0.62, P < 0.02) and plasma renin ( r = 0.55, P < 0.04). Plasma angiotensinogen decreased in infarct animals, but myocardial angiotensinogen was not different from shams (1.1 ± 0.08 vs. 2.03 ± 0.06 nM/ml plasma, P < 0.002; and 0.081 ± 0.008 vs. 0.070 ± 0.004 nM/g myocardium, respectively). In conclusion, myocardial renin increased after infarction in proportion to plasma renin and infarct size, and myocardial angiotensinogen was maintained after infarction despite decreased plasma angiotensinogen and increased levels of myocardial renin.
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Chen, Yintao, Ye Chang, Naijin Zhang, Xiaofan Guo, Guozhe Sun i Yingxian Sun. "Atorvastatin Attenuates Myocardial Hypertrophy in Spontaneously Hypertensive Rats via the C/EBPβ/PGC-1α/UCP3 Pathway". Cellular Physiology and Biochemistry 46, nr 3 (2018): 1009–18. http://dx.doi.org/10.1159/000488832.
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Background/Aims: Many clinical and experimental studies have shown that treatment with statins could prevent myocardial hypertrophy and remodeling induced by hypertension and myocardial infarction. But the molecular mechanism was not clear. We aimed to investigate the beneficial effects of atorvastatin on hypertension-induced myocardial hypertrophy and remodeling in spontaneously hypertensive rats (SHR) with the hope of revealing other potential mechanisms or target pathways to interpret the pleiotropic effects of atorvastatin on myocardial hypertrophy. Methods: The male and age-matched animals were randomly divided into three groups: control group (8 WKY), SHR (8 rats) and intervention group (8 SHR). The SHR in intervention group were administered by oral gavage with atorvastatin (suspension in distilled water, 10 mg/Kg once a day) for 6 weeks, and the other two groups were administered by gavage with equal quantity distilled water. Blood pressure of rats was measured every weeks using a standard tail cuff sphygmomanometer. Left ventricular (LV) dimensions were measured from short-axis views of LV under M-mode tracings using Doppler echocardiograph. Cardiomyocyte apoptosis was assessed by the TUNEL assay. The protein expression of C/EBPβ, PGC-1α and UCP3 were detected by immunohistochemistry or Western blot analysis. Results: At the age of 16 weeks, the mean arterial pressure of rats in three groups were 103.6±6.1, 151.8±12.5 and 159.1±6.2 mmHg respectively, and there wasn’t statistically significant difference between the SHR and intervention groups. Staining with Masson’s trichrome demonstrated that the increased interstitial fibrosis of LV and ventricular remodeling in the SHR group were attenuated by atorvastatin treatment. Echocardiography examination exhibited that SHR with atorvastatin treatment showed an LV wall thickness that was obviously lower than that of water-treated SHR. In hypertrophic myocardium, accompanied by increasing C/EBPβ expression and the percentage of TUNEL-positive cells, the expression of Bcl-2/Bax ratio, PGC-1α and UCP3 were reduced, all of which could be abrogated by treatment with atorvastatin for 6 weeks. Conclusion: This study further confirmed that atorvastatin could attenuate myocardial hypertrophy and remodeling in SHR by inhibiting apoptosis and reversing changes in mitochondrial metabolism. The C/EBPβ/PGC-1α/UCP3 signaling pathway might also be important for elucidating the beneficial pleiotropic effects of atorvastatin on myocardial hypertrophy.
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Han, Jibo, Shanshan Dai, Lingfeng Zhong, Xiaowen Shi, Xiaoxi Fan, Xin Zhong, Wante Lin i in. "GSDMD (Gasdermin D) Mediates Pathological Cardiac Hypertrophy and Generates a Feed-Forward Amplification Cascade via Mitochondria-STING (Stimulator of Interferon Genes) Axis". Hypertension 79, nr 11 (listopad 2022): 2505–18. http://dx.doi.org/10.1161/hypertensionaha.122.20004.
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Background: Cardiac hypertrophy is initially an adaptive response of cardiomyocytes to neurohumoral or hemodynamic stimuli. Evidence indicates that Ang II (angiotensin II) or pressure overload causes GSDMD (gasdermin D) activation in cardiomyocytes and myocardial tissues. However, the direct impact of GSDMD on cardiac hypertrophy and its underlying mechanisms are not fully understood. Methods and Results: In this study, we examined the aberrant activation of GSDMD in mouse and human hypertrophic myocardia, and the results showed that GSDMD deficiency reduced Ang II or pressure overload–induced cardiac hypertrophy, dysfunction, and associated cardiomyocyte pyroptosis in mice. Mechanistically, Ang II–mediated GSDMD cleavage caused mitochondrial dysfunction upstream of STING (stimulator of interferon genes) activation in vivo and in vitro. Activation of STING, in turn, potentiated GSDMD-mediated cardiac hypertrophy. Moreover, deficiency of both GSDMD and STING suppressed cardiac hypertrophy in cardiac-specific GSDMD-overexpressing mice. Conclusions: Based on these findings, we propose a mechanism by which GSDMD generates a self-amplifying, positive feed-forward loop with the mitochondria-STING axis. This finding points to the prospects of GSDMD as a key therapeutic target for hypertrophy-associated heart diseases.
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Shen, Linyuan, Mailin Gan, Zhengdong Tan, Dongmei Jiang, Yanzhi Jiang, Mingzhou Li, Jinyong Wang, Xuewei Li, Shunhua Zhang i Li Zhu. "A Novel Class of tRNA-Derived Small Non-Coding RNAs Respond to Myocardial Hypertrophy and Contribute to Intergenerational Inheritance". Biomolecules 8, nr 3 (16.07.2018): 54. http://dx.doi.org/10.3390/biom8030054.
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tRNA-derived fragments (tRFs) are a new class of non-coding RNA that play an important role in regulating cellular RNA processing and protein translation. However, there is currently no study reporting the influence of tRFs on myocardial hypertrophy. In this study, we used an isoproterenol (ISO)-induced myocardial hypertrophy rat model. Small RNA (<40 nts) transcriptome sequencing was used to select differentially expressed tRFs. We also compared the tRFs expression pattern in F0 sperm and the hearts of F1 offspring between the myocardial hypertrophy group (Hyp) and the control group (Con). Isoproterenol successfully induced a typical cardiac hypertrophy model in our study. Small RNA-seq revealed that tRFs were extremely enriched (84%) in the Hyp heart. Overexpression of tRFs1 and tRFs2 both enlarged the surface area of cardiac cells and increased expression of hypertrophic markers (ANF, BNP, and β-MHC). Luciferase reporter assay identified that tRFs1 directly target 3′UTR of Timp3. tRFs1, tRFs2, tRFs3, and tRFs4 were also highly expressed in Hyp F0 sperm and in Hyp F1 offspring hearts, but there was no differential expression of tRFs7, tRFs9, and tRFs10. Compared to Con F1 offspring, Hyp F1 offspring had elevated expression levels of β-MHC and ANP genes, and they had increased fibrosis and apoptosis in their hearts. These results demonstrated that tRFs are involved in regulating the response of myocardial hypertrophy. Besides, tRFs might serve as novel epigenetic factors that contribute to the intergenerational inheritance of cardiac hypertrophy.
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Tsuda, Takeshi. "Clinical Assessment of Ventricular Wall Stress in Understanding Compensatory Hypertrophic Response and Maladaptive Ventricular Remodeling". Journal of Cardiovascular Development and Disease 8, nr 10 (29.09.2021): 122. http://dx.doi.org/10.3390/jcdd8100122.
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Ventricular wall stress (WS) is an important hemodynamic parameter to represent myocardial oxygen demand and ventricular workload. The normalization of WS is regarded as a physiological feedback signal that regulates the rate and extent of ventricular hypertrophy to maintain myocardial homeostasis. Although hypertrophy is an adaptive response to increased biomechanical stress, persistent hypertrophic stimulation forces the stressed myocardium into a progressive maladaptive process called ventricular remodeling, consisting of ventricular dilatation and dysfunction in conjunction with the development of myocyte hypertrophy, apoptosis, and fibrosis. The critical determinant of this pathological transition is not fully understood, but an energetic mismatch due to uncontrolled WS is thought to be a central mechanism. Despite extensive basic investigations conducted to understand the complex signaling pathways involved in this maladaptive process, clinical diagnostic studies that translate these molecular and cellular changes are relatively limited. Echocardiographic assessment with or without direct measurement of left ventricular pressure used to be a mainstay in estimating ventricular WS in clinical medicine, but in recent years more and more noninvasive applications with magnetic resonance imaging have been studied. In this review article, basic clinical applications of WS assessment are discussed to help understand the progression of ventricular remodeling.
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Dung, Van Hung, Pham Thanh Binh, Nguyen Tien Hoa i Bui Minh Trang. "Case report: Bilateral hypertrophic obstructive cardiomyophathy associated with myocardial bridge". Tạp chí Phẫu thuật Tim mạch và Lồng ngực Việt Nam 39 (31.10.2022): 122–25. http://dx.doi.org/10.47972/vjcts.v39i.810.
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Hypertrophic obstructive cardiomyopathy is a rare cardiac disease occurring in approximately 0.2% of the population and is usually left ventricular hypertrophy associated with or without mitral regurgitation due to SAM syndrome. Medical treatment, first septal ablation with absolute alcohol, or left ventricular myectomy are the treatment methods for this disease. We report the surgical results of a case of obstructive bilateral ventricular hypertrophy associated with a myocardial bridging of the left anterior descending artery.
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Tennant, Bryn. "Small Animal Review". Companion Animal 25, nr 5 (2.06.2020): 110. http://dx.doi.org/10.12968/coan.2020.0043.
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Summary: In feline hypertrophic cardiomyopathy the increase in myocardial thickness and cardiac weight in some cases is due to diffuse expansion of the interstitium by granulation tissue as a consequence of cardiomyocyte degeneration, probably associated with infarcts, and is not necessarily the result of true myocardial hypertrophy.
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Strøm, Claes C., Mogens Kruhøffer, Steen Knudsen, Frank Stensgaard-Hansen, Thomas E. N. Jonassen, Torben F. Ørntoft, Stig Haunsø i Søren P. Sheikh. "Identification of a Core Set of Genes That Signifies Pathways Underlying Cardiac Hypertrophy". Comparative and Functional Genomics 5, nr 6-7 (2004): 459–70. http://dx.doi.org/10.1002/cfg.428.
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Although the molecular signals underlying cardiac hypertrophy have been the subject of intense investigation, the extent of common and distinct gene regulation between different forms of cardiac hypertrophy remains unclear. We hypothesized that a general and comparative analysis of hypertrophic gene expression, using microarray technology in multiple models of cardiac hypertrophy, including aortic banding, myocardial infarction, an arteriovenous shunt and pharmacologically induced hypertrophy, would uncover networks of conserved hypertrophy-specific genes and identify novel genes involved in hypertrophic signalling. From gene expression analyses (8740 probe sets,n= 46) of rat ventricular RNA, we identified a core set of 139 genes with consistent differential expression in all hypertrophy models as compared to their controls, including 78 genes not previously associated with hypertrophy and 61 genes whose altered expression had previously been reported. We identified a single common gene program underlying hypertrophic remodelling, regardless of how the hypertrophy was induced. These genes constitute the molecular basis for the existence of one main form of cardiac hypertrophy and may be useful for prediction of a common therapeutic approach. Supplementary material for this article can be found at: http://www.interscience.wiley.com/jpages/1531-6912/suppmat
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Lorén, Christina, Christen Dahl, Lan Do, Vibeke Almaas, Odd Geiran, Stellan Mörner i Urban Hellman. "Low Molecular Mass Myocardial Hyaluronan in Human Hypertrophic Cardiomyopathy". Cells 8, nr 2 (29.01.2019): 97. http://dx.doi.org/10.3390/cells8020097.
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During the development of hypertrophic cardiomyopathy, the heart returns to fetal energy metabolism where cells utilize more glucose instead of fatty acids as a source of energy. Metabolism of glucose can increase synthesis of the extracellular glycosaminoglycan hyaluronan, which has been shown to be involved in the development of cardiac hypertrophy and fibrosis. The aim of this study was to investigate hyaluronan metabolism in cardiac tissue from patients with hypertrophic cardiomyopathy in relation to cardiac growth. NMR and qRT-PCR analysis of human cardiac tissue from hypertrophic cardiomyopathy patients and healthy control hearts showed dysregulated glucose and hyaluronan metabolism in the patients. Gas phase electrophoresis revealed a higher amount of low molecular mass hyaluronan and larger cardiomyocytes in cardiac tissue from patients with hypertrophic cardiomyopathy. Histochemistry showed high concentrations of hyaluronan around individual cardiomyocytes in hearts from hypertrophic cardiomyopathy patients. Experimentally, we could also observe accumulation of low molecular mass hyaluronan in cardiac hypertrophy in a rat model. In conclusion, the development of hypertrophic cardiomyopathy with increased glucose metabolism affected both hyaluronan molecular mass and amount. The process of regulating cardiomyocyte size seems to involve fragmentation of hyaluronan.
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Basargina, E. N., V. S. Ermolenko i I. V. Sil’nova. "Myocardial hypertrophy in infants in pediatric practice". Kazan medical journal 96, nr 4 (15.08.2015): 647–53. http://dx.doi.org/10.17750/kmj2015-647.
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Aim. To identify the features of the diseases associated with myocardial hypertrophy, for an earlier differential diagnosis to determine the treatment tactics and to initiate the early treatment.
Methods. Clinical examination, family history, cardiac ultrasound with Doppler, ECG, 24-hour ECG monitoring, and computed tomographic aortography and genetics counseling (if indicated) were preformed.
Results. During 14 years of observations, 92 patients were included, among them: children with idiopathic hypertrophic cardiomyopathy - 49 (53%), followed by children with Noonan syndrome - 11 (11.9%), Pompe disease - 6 (6.5%), hypertension - 6 (6.5%), Leopard syndrome - 5 (5,4%), Friedrich ataxia - 4 (4.3%), Danon disease - 3 (3.2%), cardiofaciocutaneous syndrome, fatty acids beta-oxidation disorder and mucopolysaccharidosis type I (Hurler syndrome) - 2 (2.1%), carnitine deficiency and GM1-gangliosidosis - 1 (1.2%).
Conclusion. Consudering the possibilities of modern medicine, diagnosis of left and/or right ventricular hypertrophy in pediatric general practice and pediatric cardiology is an important factor for the subsequent diagnostic search, earliest possible specific therapeutic interventions to prevent unfavorable outcomes of the diseases.
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Zhu, Huiping, Liutong Pan, Yuanting Dai, Dan Zheng i Shasha Cai. "Role of TLR4/MyD88 Signaling Pathway in the Occurrence and Development of Uremia-Induced Myocardial Hypertrophy and Possible Mechanism". Evidence-Based Complementary and Alternative Medicine 2021 (13.10.2021): 1–9. http://dx.doi.org/10.1155/2021/7883643.
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The morbidity and mortality of cardiovascular disease (CVD) are relatively high. Studies have shown that most patients with chronic kidney disease (CKD) die from cardiovascular complications. Clinically, the pathophysiological state in which heart disease and kidney disease are causal and influence each other is called cardiorenal syndrome (CRS). Myocardial hypertrophy is the key stage of the heart structure changing from reversible to irreversible. It is an important pathophysiological basis for heart failure. Therefore, this study intends to start with the end-stage uremic phase of CKD to construct an animal model of uremia in rats to study the relationship between uremia, TLR4/MyD88 signaling pathway, and myocardial hypertrophy. The results showed that the uremic rats showed slow weight gain and were thinner. At 12 weeks (w), the serum creatinine and urea nitrogen of the uremic rats increased, and the global hypertrophy index increased. Detecting the expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor (MyD88) in blood samples of rats, we found that the expression of TLR4 and MyD88 increased at 12 w in the uremia group; pathological observation showed that at 4 weeks of uremia model rats, renal tissue compensatory hypertrophy, renal fibrous membrane proliferation, renal parenchyma atrophy, a large number of fibrous proliferation and inflammatory cell infiltration in the interstitium, and protein casts in the renal tubules were observed. Myocardial cells were obviously hypertrophy and disordered. At 12 w, renal tubules were obviously expanded, the epithelium was flat, the brush border disappeared, and the interstitial fibrous connective tissue of the myocardial tissue was proliferated. The detection of TLR4 and MyD88 in kidney tissue and myocardial tissue revealed that the positive expression of TLR4 and MyD88 gradually increased over time. Therefore, the final result of the study is that uremia can gradually lead to myocardial hypertrophy and TLR4 and MyD88 are highly expressed in serum, kidney, and myocardial tissues of uremic rats, suggesting that TLR4 and MyD88 may be related to the degree of uremic disease and the myocardium caused by it. Hypertrophy is related.
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Calamaras, Timothy D., Robert A. Baumgartner, Mark J. Aronovitz, Angela L. McLaughlin, Kelly Tam, Daniel A. Richards, Craig W. Cooper i in. "Mixed lineage kinase-3 prevents cardiac dysfunction and structural remodeling with pressure overload". American Journal of Physiology-Heart and Circulatory Physiology 316, nr 1 (1.01.2019): H145—H159. http://dx.doi.org/10.1152/ajpheart.00029.2018.
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Myocardial hypertrophy is an independent risk factor for heart failure (HF), yet the mechanisms underlying pathological cardiomyocyte growth are incompletely understood. The c-Jun NH2-terminal kinase (JNK) signaling cascade modulates cardiac hypertrophic remodeling, but the upstream factors regulating myocardial JNK activity remain unclear. In this study, we sought to identify JNK-activating molecules as novel regulators of cardiac remodeling in HF. We investigated mixed lineage kinase-3 (MLK3), a master regulator of upstream JNK-activating kinases, whose role in the remodeling process had not previously been studied. We observed increased MLK3 protein expression in myocardium from patients with nonischemic and hypertrophic cardiomyopathy and in hearts of mice subjected to transverse aortic constriction (TAC). Mice with genetic deletion of MLK3 (MLK3−/−) exhibited baseline cardiac hypertrophy with preserved cardiac function. MLK3−/− mice subjected to chronic left ventricular (LV) pressure overload (TAC, 4 wk) developed worsened cardiac dysfunction and increased LV chamber size compared with MLK3+/+ littermates ( n = 8). LV mass, pathological markers of hypertrophy ( Nppa, Nppb), and cardiomyocyte size were elevated in MLK3−/− TAC hearts. Phosphorylation of JNK, but not other MAPK pathways, was selectively impaired in MLK3−/− TAC hearts. In adult rat cardiomyocytes, pharmacological MLK3 kinase inhibition using URMC-099 blocked JNK phosphorylation induced by neurohormonal agents and oxidants. Sustained URMC-099 exposure induced cardiomyocyte hypertrophy. These data demonstrate that MLK3 prevents adverse cardiac remodeling in the setting of pressure overload. Mechanistically, MLK3 activates JNK, which in turn opposes cardiomyocyte hypertrophy. These results support modulation of MLK3 as a potential therapeutic approach in HF. NEW & NOTEWORTHY Here, we identified a role for mixed lineage kinase-3 (MLK3) as a novel antihypertrophic and antiremodeling molecule in response to cardiac pressure overload. MLK3 regulates phosphorylation of the stress-responsive JNK kinase in response to pressure overload and in cultured cardiomyocytes stimulated with hypertrophic agonists and oxidants. This study reveals MLK3-JNK signaling as a novel cardioprotective signaling axis in the setting of pressure overload.
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Zhao, Mingyue, Lihui Lu, Song Lei, Hua Chai, Siyuan Wu, Xiaoju Tang, Qinxue Bao, Li Chen, Wenchao Wu i Xiaojing Liu. "Inhibition of Receptor Interacting Protein Kinases Attenuates Cardiomyocyte Hypertrophy Induced by Palmitic Acid". Oxidative Medicine and Cellular Longevity 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/1451676.
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Palmitic acid (PA) is known to cause cardiomyocyte dysfunction. Cardiac hypertrophy is one of the important pathological features of PA-induced lipotoxicity, but the mechanism by which PA induces cardiomyocyte hypertrophy is still unclear. Therefore, our study was to test whether necroptosis, a receptor interacting protein kinase 1 and 3 (RIPK1 and RIPK3-) dependent programmed necrosis, was involved in the PA-induced cardiomyocyte hypertrophy. We used the PA-treated primary neonatal rat cardiac myocytes (NCMs) or H9c2 cells to study lipotoxicity. Our results demonstrated that cardiomyocyte hypertrophy was induced by PA treatment, determined by upregulation of hypertrophic marker genes and cell surface area enlargement. Upon PA treatment, the expression of RIPK1 and RIPK3 was increased. Pretreatment with the RIPK1 inhibitor necrostatin-1 (Nec-1), the PA-induced cardiomyocyte hypertrophy, was attenuated. Knockdown of RIPK1 or RIPK3 by siRNA suppressed the PA-induced myocardial hypertrophy. Moreover, a crosstalk between necroptosis and endoplasmic reticulum (ER) stress was observed in PA-treated cardiomyocytes. Inhibition of RIPK1 with Nec-1, phosphorylation level of AKT (Ser473), and mTOR (Ser2481) was significantly reduced in PA-treated cardiomyocytes. In conclusion, RIPKs-dependent necroptosis might be crucial in PA-induced myocardial hypertrophy. Activation of mTOR may mediate the effect of necroptosis in cardiomyocyte hypertrophy induced by PA.
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Ming, Sitong, Mo Kan, Liu Liu, Zhuang Zhang, Xiaoran Liu, Yaxin Liu, Zhen Li i in. "Protective Effect of Shengmaiyin in Myocardial Hypertrophy-Induced Rats: A Genomic Analysis by 16S rDNA". Evidence-Based Complementary and Alternative Medicine 2022 (7.09.2022): 1–17. http://dx.doi.org/10.1155/2022/3188292.
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Background. The gut-cardiac axis theory provides new insights into the complex mechanisms of cardiac hypertrophy and provides new therapeutic targets. Cardiac hypertrophy is a risk factor for heart failure. Shengmaiyin (SMY) is a traditional Chinese medicine formula with clear effects in the treatment and prevention of cardiac hypertrophy, but the mechanism by which it improves cardiac hypertrophy is still unclear. Therefore, this study aimed to investigate the protective effect and mechanism of SMY on isoproterenol (ISO)-induced myocardial hypertrophy in rats. Methods. First, various pharmacodynamic methods were used to evaluate the therapeutic effect of SMY on ISO-induced myocardial hypertrophy in rats. Then, 16S rDNA amplicon sequencing technology was used to study the effect of SMY on the intestinal flora of rats with myocardial hypertrophy. Finally, the mechanism underlying the effect of SMY on cardiac hypertrophy was predicted by bioinformatics network analysis and verified by Western blotting. Results. SMY increased ejection fraction (EF%) and left ventricular fractional shortening (FS%), ameliorated myocardial cell injury and fibrosis, regulated blood lipids and energy metabolism, and decreased cardiac hypertrophy marker gene expression. The gut microbiota of ISO-induced myocardial hypertrophy rats were significantly changed, while SMY effectively ameliorated the dysbiosis of the intestinal flora in rats with myocardial hypertrophy, especially Prevotella 9, Lactobacillus, and Clostridium. Mechanistic studies have shown that the anticardiac hypertrophy effect of SMY is related to the inhibition of the expression of HIF1α/PPAR signalling pathway-related proteins. Conclusion. SMY significantly improves cardiac function, relieves myocardial cell fibrosis and necrosis, resists cardiac hypertrophy, improves blood lipid metabolism and energy metabolism, regulates intestinal microbial disturbance, and protects the heart.
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Sharma, Jayendra, William Hellenbrand, Charles Kleinman i Ralph Mosca. "Symptomatic myocardial bridges in children: a case report with review of literature". Cardiology in the Young 21, nr 5 (23.06.2011): 490–94. http://dx.doi.org/10.1017/s1047951111000849.
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AbstractMyocardial bridge is a rare congenital coronary anomaly in children, usually seen in the setting of hypertrophic cardiomyopathy and in left ventricular hypertrophy. Most myocardial bridges are believed to represent a benign anatomical variant; however, symptomatic myocardial bridge is a distinct subgroup of pathological variant, linked to myocardial ischaemia, ventricular arrhythmia, and sudden cardiac death. We present a case of a symptomatic myocardial bridge in a 5-year-old boy with mild hypertrophic cardiomyopathy who underwent supra-arterial myotomy, automatic defibrillator placement, and long-term Beta-blocker therapy. We also present 10 years of follow-up with a review of literature regarding symptomatic myocardial bridges in the paediatric age group.
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Jain, Mohit, Ronglih Liao, Bruno K. Podesser, Soeun Ngoy, Carl S. Apstein i Franz R. Eberli. "Influence of gender on the response to hemodynamic overload after myocardial infarction". American Journal of Physiology-Heart and Circulatory Physiology 283, nr 6 (1.12.2002): H2544—H2550. http://dx.doi.org/10.1152/ajpheart.00338.2002.
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After myocardial infarction (MI), the left ventricle (LV) undergoes ventricular remodeling characterized by progressive global dilation, infarct expansion, and compensatory hypertrophy of the noninfarcted myocardium. Little attention has been given to the response of remodeling myocardium to additional hemodynamic overload. Studies have indicated that gender may influence remodeling and the response to both MI and hemodynamic overload. We therefore determined 1) structural and function consequences of superimposing hemodynamic overload (systemic hypertension) on remodeling myocardium after a MI and 2) the potential influence of gender on this remodeling response. Male and female Dahl salt-sensitive and salt-resistant rats underwent coronary ligation, resulting in similar degrees of MI. One week post-MI, all rats were placed on a high-salt diet. Four groups were then studied 4 wk after initiation of high-salt feeding: MI female, MI female + hypertension, MI male, and MI male + hypertension. Hypertension-induced pressure overload resulted in additional comparable degrees of myocardial hypertrophy in both females and males. In females, hypertension post-MI resulted in concentric hypertrophy with no additional cavity dilation and no measurable scar thinning. In contrast, in males, hypertension post-MI resulted in eccentric hypertrophy, further LV cavity dilation, and scar thinning. Physiologically, concentric hypertrophy in post-MI hypertensive females resulted in elevated contractile function, whereas eccentrically hypertrophied males had no such increase. Female gender influences favorably the remodeling and physiological response to hemodynamic overload after large MI.
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Katz, Stephen A., John A. Opsahl, Shane E. Wernsing, Lynn M. Forbis, Juline Smith i Lois J. Heller. "Myocardial renin is neither necessary nor sufficient to initiate or maintain ventricular hypertrophy". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, nr 3 (1.03.2000): R578—R586. http://dx.doi.org/10.1152/ajpregu.2000.278.3.r578.
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We tested the hypothesis that the myocardial renin-angiotensin system (RAS) is both necessary and sufficient to initiate and maintain all classes of ventricular hypertrophy. Myocardial and plasma renin and angiotensinogen were measured in rats during initiation and maintenance of ventricular hypertrophy associated with DOCA implants and 1% NaCl drinking water, with and without the AT1 ANG II receptor blocker losartan. Additional groups of rats were given a low-sodium diet (0.04%) for 3 wk. Ventricular hypertrophy was initiated within 7 days and maintained for 35 days in DOCA-treated rats despite significantly low myocardial and plasma renin, normal or low myocardial and plasma angiotensinogen, or the presence of losartan. Furthermore, there was no ventricular hypertrophy in low-salt diet-fed animals despite increased myocardial and plasma renin levels and normal angiotensinogen levels. Therefore, the myocardial RAS is not necessary to initiate or maintain cardiac hypertrophy in DOCA-treated rats and is not sufficient to initiate cardiac hypertrophy in low-salt diet-fed rats. Additionally, myocardial renin and angiotensinogen were significantly correlated with corresponding plasma levels.
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Sarkar, Sagartirtha, Douglas W. Leaman, Sudhiranjan Gupta, Parames Sil, David Young, Annitta Morehead, Debabrata Mukherjee i in. "Cardiac Overexpression of Myotrophin Triggers Myocardial Hypertrophy and Heart Failure in Transgenic Mice". Journal of Biological Chemistry 279, nr 19 (16.02.2004): 20422–34. http://dx.doi.org/10.1074/jbc.m308488200.
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Cardiac hypertrophy and heart failure remain leading causes of death in the United States. Many studies have suggested that, under stress, myocardium releases factors triggering protein synthesis and stimulating myocyte growth. We identified and cloned myotrophin, a 12-kDa protein from hypertrophied human and rat hearts. Myotrophin (whose gene is localized on human chromosome 7q33) stimulates myocyte growth and participates in cellular interaction that initiates cardiac hypertrophyin vitro. In this report, we present data on the pathophysiological significance of myotrophinin vivo, showing the effects of overexpression of cardio-specific myotrophin in transgenic mice in which cardiac hypertrophy occurred by 4 weeks of age and progressed to heart failure by 9-12 months. This hypertrophy was associated with increased expression of proto-oncogenes, hypertrophy marker genes, growth factors, and cytokines, with symptoms that mimicked those of human cardiomyopathy, functionally and morphologically. This model provided a unique opportunity to analyze gene clusters that are differentially up-regulated during initiation of hypertrophyversustransition of hypertrophy to heart failure. Importantly, changes in gene expression observed during initiation of hypertrophy were significantly different from those seen during its transition to heart failure. Our data show that overexpression of myotrophin results in initiation of cardiac hypertrophy that progresses to heart failure, similar to changes in human heart failure. Knowledge of the changes that take place as a result of overexpression of myotrophin at both the cellular and molecular levels will suggest novel strategies for treatment to prevent hypertrophy and its progression to heart failure.
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Liu, Lei, Chao Wang, Dianjun Sun, Shuangquan Jiang, Hong Li, Weihua Zhang, Yajun Zhao i in. "Calhex231 Ameliorates Cardiac Hypertrophy by Inhibiting Cellular Autophagy in Vivo and in Vitro". Cellular Physiology and Biochemistry 36, nr 4 (2015): 1597–612. http://dx.doi.org/10.1159/000430322.
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Background/Aims: Intracellular calcium concentration ([Ca2+]i) homeostasis, an initial factor of cardiac hypertrophy, is regulated by the calcium-sensing receptor (CaSR) and is associated with the formation of autolysosomes. The aim of this study was to investigate the role of Calhex231, a CaSR inhibitor, on the hypertrophic response via autophagy modulation. Methods: Cardiac hypertrophy was induced by transverse aortic constriction (TAC) in 40 male Wistar rats, while 10 rats underwent a sham operation and served as controls. Cardiac function was monitored by transthoracic echocardiography, and the hypertrophy index was calculated. Cardiac tissue was stained with hematoxylin and eosin (H&E) or Masson's trichrome reagent and examined by transmission electron microscopy. An angiotensin II (Ang II)-induced cardiomyocyte hypertrophy model was established and used to test the involvement of active molecules. Intracellular calcium concentration ([Ca2+]i) was determined by the introduction of Fluo-4/AM dye followed by confocal microscopy. The expression of various active proteins was analyzed by western blot. Results: The rats with TAC-induced hypertrophy had an increased heart size, ratio of heart weight to body weight, myocardial fibrosis, and CaSR and autophagy levels, which were suppressed by Calhex231. Experimental results using Ang II-induced hypertrophic cardiomyocytes confirmed that Calhex231 suppressed CaSR expression and downregulated autophagy by inhibiting the Ca2+/calmodulin-dependent-protein kinase-kinase-β (CaMKKβ)- AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) pathway to ameliorate cardiomyocyte hypertrophy. Conclusions: Calhex231 ameliorates myocardial hypertrophy induced by pressure-overload or Ang II via inhibiting CaSR expression and autophagy. Our results may support the notion that Calhex231 can become a new therapeutic agent for the treatment of cardiac hypertrophy.
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Iswara, Raja Al Fath Widya, Arif Rahman Sadad, Intarniati Nur Rohmah i Sigid Kirana Lintang Bhima. "Kematian Mendadak Akibat Kardiomiopati Hipertrofi Pada Dewasa Muda". Medica Hospitalia : Journal of Clinical Medicine 7, nr 2 (19.11.2020): 470–75. http://dx.doi.org/10.36408/mhjcm.v7i2.522.
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Latar Belakang : Kematian mendadak merupakan kasus yang paling sering terjadi dan dapat ditemukan dalam berbagai macam kondisi. Penyebab kematian mendadak terbanyak adalah sistem kardiovaskular dan salah satu kelainan yang jarang terjadi adalah kardiomiopati hipertrofi. Kardiomiopati hipertrofi merupakan kelainan jantung yang ditandai dengan hipertrofi miokardial akibat mutasi sarkomer dengan angka kejadian 1 dari 500 orang dewasa. Temuan utama pada kardiomiopati hipertrofi antara lain adanya hipertofi ventrikel dan atau septum interventrikel, kerusakan miosit dan peningkatan fibrosis miokardium. Terdapat variasi manifestasi klinis pada Kardiomiopati hipertrofi, dari asimptomatik hingga mengakibatkan kematian mendadak akibat gagal jantung. Tujuan laporan kasus ini adalah mengetahui diagnosis kematian akibat kardiomiopati hipertrofi pada dewasa muda.
Kasus : Seorang laki-laki usia 18 tahun ditemukan meninggal di kamar kostannya dibawa ke kamar jenazah RSUP dr. Kariadi Semarang untuk diotopsi. Pemeriksaan luar tidak ditemukan tanda-tanda kekerasan. Pemeriksaan dalam didapatkan adanya jendalan darah dalam ventrikel, hipertrofi ventrikel kiri, penebalan pada katub jantung, pengerasan pada otot jantung dan penggantung katub serta tanda asfiksia. Pemeriksaan histopatologi menunjukkan kardiomiopati hipertrofi.
Pembahasan : Patogenesis kardiomiopati hipertrofi dapat menyebabkan asfiksia yaitu terjadinya mutasi intrasarkomer yang meningkatkan peningkatan sensitivitas dan produksi Calsium yang mengakibatkan peningkatan kontraksi miokardium sehingga menyebabkan hipertrofi ventrikel kiri. Selain itu juga terjadi peningkatan sintesis kolagen yang mengakibatkan terjadinya fibrosis miokard yang menyebabkan hipertrofi ventrikel kiri. Terjadinya hipertrofi ventrikel kiri jangka panjang akan menyebabkan kondisi gagal jantung yang dapat mengakibatkan asfiksia.
Simpulan : Kematian mendadak akibat kardiomiopati hipertrofi merupakan hal yang jarang. Oleh karena itu dibutuhkan otopsi yang teliti dan pemeriksaan histopatologi untuk mendiagnosis dengan pasti.
Kata Kunci : Kematian mendadak, kardiomiopati hipertrofi, dewasa muda, sarkomer
Background : Sudden death is the most common case and can be found in a variety of conditions. The most common cause of death is the cardiovascular system and a rare one disorders is hypertrophic cardiomyopathy. Hypertrophy cardiomyopathy is a heart disorder characterized by myocardial hypertrophy due to sarcomere mutations with an incidence of 1 in 500 adults. The main findings in hypertrophic cardiomyopathy include the presence of ventricular hypertrophy and / or interventricular septum, myocyte damage and increased myocardial fibrosis. There are variations in clinical manifestations in hypertrophic cardiomyopathy, from asymptomatic to sudden death due to heart failure. The purpose of this case report is to know the diagnosis of sudden death due to hypertrophic cardiomyopathy in young adults
Case : A 18-year-old man was found dead in his boarding room. On the external examination there were no signs of violence. On the internal examination in the presence of blood in the ventricles, left ventricular hypertrophy, thickening of the entire heart valve, hardening of the heart muscle and hanging valves and signs of asphyxia. Histopathological examination showed hypertrophic cardiomyopathy.
Discussion : The pathogenesis of hypertrophic cardiomyopathy can cause asphyxia is the occurrence of intrasarcomere mutations that increase the sensitivity and production of calcium which results in increased contraction of the myocardium causing left ventricular hypertrophy. In addition there is also an increase in collagen synthesis which results in the occurrence of myocardial fibrosis which causes left ventricular hypertrophy. The occurrence of long-term left ventricular hypertrophy will cause a condition of heart failure which can lead to asphyxia.
Conclusion : Sudden death due to hypertrophic cardiomyopathy is rare one. Therefore a careful autopsy is needed and histopathological examination is needed to get definitive diagnose.
Keywords : Sudden death, hypertrophic cardiomyopathy, young adults, sarcomere
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Sui, Xin, Na Li, Xiaozheng Shi, Xiaohua Li, Dong Han, Zhidong Qiu, Yue Deng i Guangwei Sun. "Pinocembrin Protects Cardiomyocytes Against Isoproterenol-Induced Hypertrophy". Natural Product Communications 16, nr 8 (sierpień 2021): 1934578X2110332. http://dx.doi.org/10.1177/1934578x211033216.
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Cardiac hypertrophy is characterized by an increase in myocardial cell volume and extracellular matrix production. Persistent cardiac hypertrophy can cause dilated cardiomyopathy, heart failure, and even death. Pinocembrin (5,7-dihydroxyflavanone) is a type of flavonoid, extracted from propolis, that has antimicrobial, antioxidant, antiinflammatory, and anticancer properties. The results of the present study showed that pretreatment of isoproterenol (ISO)-treated H9c2 cardiomyocytes with pinocembrin reduced the messenger RNA levels of hypertrophic markers, including atrial natriuretic factor and βeta-myosin heavy chain, and inflammatory cytokines, such as tumor necrosis factor-α, interleukin-6, interleukin-1β, and interferon-γ, and also inhibited p65 phosphorylation and nuclear factor-kappa B (NF-κB) translocation. In addition, the activity of IκBα, an inhibitor of NF-κB, was increased while that of caspase-3 was reduced under these conditions. These results indicate that pinocembrin may inhibit ISO-induced myocardial hypertrophy by attenuating the NF-κB signaling pathway.
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García-Díaz, Lutgardo, Félix Coserria i Guillermo Antiñolo. "Hypertrophic Cardiomyopathy due to Mitochondrial Disease: Prenatal Diagnosis, Management, and Outcome". Case Reports in Obstetrics and Gynecology 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/472356.
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A case of prenatally diagnosed fetal hypertrophic cardiomyopathy is reported. The mother was referred to our department at 37 weeks' gestation because of suspected congenital heart disease. Prenatal echocardiography showed biventricular hypertrophy and pericardial effusion, without additional abnormalities. Postnatal echocardiography confirmed prenatal diagnosis. Neonatal EKG showed biventricular hypertrophy and Wolff-Parkinson-White syndrome. Skeletal muscle biopsy was consistent with mitochondrial oxidative phosphorylation defect involving a combined defect of respiratory complexes I and IV. Echocardiographic followup during the first year of life showed progressive regression of hypertrophy and evolution to left ventricular myocardial noncompaction.
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Bupha-Intr, Tepmanas, Jeffrey W. Holmes i Paul M. L. Janssen. "Induction of hypertrophy in vitro by mechanical loading in adult rabbit myocardium". American Journal of Physiology-Heart and Circulatory Physiology 293, nr 6 (grudzień 2007): H3759—H3767. http://dx.doi.org/10.1152/ajpheart.01267.2006.
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To study myocardial hypertrophy under in vitro conditions, we developed an experimental system and protocol in which mechanical conditions of isolated multicellular myocardium can be controlled while function can be continuously assessed. This in vitro culture system now allows us to investigate how mechanical overload impacts on cardiac hypertrophy in the absence of systemic factors. In this system, small right ventricular rabbit trabeculae were subjected to different modes of mechanical load, while being electrically stimulated to contract at 1 Hz at 37°C. Muscles subjected to prolonged isometric contractions at high, but physiological, pre- and afterload showed a rapid induction of cardiac hypertrophy; overall muscle diameter increased by 4.3 ± 1.4 and 17.9 ± 4.0% after 24 and 48 h, respectively. This finding was confirmed at the cellular level; individual myocyte width significantly increased after 24 and 48 h. In muscles subjected to a low preload, or in the absence of afterload, this hypertrophic response was absent. Functionally, after 24 h of isometric contractions at high load, active developed tension had gradually increased to 168 ± 22% of starting values. Proteomic analysis of this cultured myocardium demonstrated reproducible changes in the protein expression pattern and included an upregulation of myofilament proteins, myosin light chain isoforms, α-b crystalline, and breast cancer 1 protein, and a downregulation of myoglobin. We conclude that multicellular myocardium can be stressed to undergo rapid hypertrophy in vitro, and changes in function and protein expression can be investigated during the transition from healthy myocardium to early hypertrophy.
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Morgan, Howard E. "Signal transduction in myocardial hypertrophy." Keio Journal of Medicine 39, nr 1 (1990): 1–5. http://dx.doi.org/10.2302/kjm.39.1.
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Zhang, Jianyi. "Myocardial Energetics In Cardiac Hypertrophy". Clinical and Experimental Pharmacology and Physiology 29, nr 4 (kwiecień 2002): 351–59. http://dx.doi.org/10.1046/j.1440-1681.2002.03657.x.
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