Academic literature on the topic 'Pathological hypertrophy'
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Journal articles on the topic "Pathological hypertrophy"
Li, Wei-ming, Yi-fan Zhao, Guo-fu Zhu, Wen-hui Peng, Meng-yun Zhu, Xue-jing Yu, Wei Chen, Da-chun Xu, and Ya-wei Xu. "Dual specific phosphatase 12 ameliorates cardiac hypertrophy in response to pressure overload." Clinical Science 131, no. 2 (December 23, 2016): 141–54. http://dx.doi.org/10.1042/cs20160664.
Full textYu, Qing, Wenxin Kou, Xu Xu, Shunping Zhou, Peipei Luan, Xiaopeng Xu, Hailing Li, et al. "FNDC5/Irisin inhibits pathological cardiac hypertrophy." Clinical Science 133, no. 5 (March 1, 2019): 611–27. http://dx.doi.org/10.1042/cs20190016.
Full textKang, Peter M., Patrick Yue, Zhilin Liu, Oleg Tarnavski, Natalya Bodyak, and Seigo Izumo. "Alterations in apoptosis regulatory factors during hypertrophy and heart failure." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 1 (July 2004): H72—H80. http://dx.doi.org/10.1152/ajpheart.00556.2003.
Full textLi, Peng-Long, Hui Liu, Guo-Peng Chen, Ling Li, Hong-Jie Shi, Hong-Yu Nie, Zhen Liu, et al. "STEAP3 (Six-Transmembrane Epithelial Antigen of Prostate 3) Inhibits Pathological Cardiac Hypertrophy." Hypertension 76, no. 4 (October 2020): 1219–30. http://dx.doi.org/10.1161/hypertensionaha.120.14752.
Full textJACOB, R., M. VOGT, and H. RUPP. "Physiological and pathological hypertrophy*." Journal of Molecular and Cellular Cardiology 18 (1986): 35. http://dx.doi.org/10.1016/s0022-2828(86)80135-3.
Full textTanaka, M., H. Fujiwara, and C. Kawai. "Pathological features of hypertrophic cardiomyopathy without asymmetrical septal hypertrophy." Heart 56, no. 3 (September 1, 1986): 294–97. http://dx.doi.org/10.1136/hrt.56.3.294.
Full textHu, Chengyun, Feibiao Dai, Jiawu Wang, Lai Jiang, Di Wang, Jie Gao, Jun Huang, et al. "Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice." Oxidative Medicine and Cellular Longevity 2022 (January 29, 2022): 1–12. http://dx.doi.org/10.1155/2022/5067544.
Full textLu, Dan, Jizheng Wang, Jing Li, Feifei Guan, Xu Zhang, Wei Dong, Ning Liu, Shan Gao, and Lianfeng Zhang. "Meox1 accelerates myocardial hypertrophic decompensation through Gata4." Cardiovascular Research 114, no. 2 (November 16, 2017): 300–311. http://dx.doi.org/10.1093/cvr/cvx222.
Full textGao, Si, Xue-ping Liu, Li-hua Wei, Jing Lu, and Peiqing Liu. "Upregulation of α-enolase protects cardiomyocytes from phenylephrine-induced hypertrophy." Canadian Journal of Physiology and Pharmacology 96, no. 4 (April 2018): 352–58. http://dx.doi.org/10.1139/cjpp-2017-0282.
Full textLuckey, Stephen W., Chris D. Haines, John P. Konhilas, Elizabeth D. Luczak, Antke Messmer-Kratzsch, and Leslie A. Leinwand. "Cyclin D2 is a critical mediator of exercise-induced cardiac hypertrophy." Experimental Biology and Medicine 242, no. 18 (September 13, 2017): 1820–30. http://dx.doi.org/10.1177/1535370217731503.
Full textDissertations / Theses on the topic "Pathological hypertrophy"
Crampton, Matthew S., and n/a. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070104.165826.
Full textCrampton, Matthew S. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/366605.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Ferreira, Linda. "A Molecular Analysis of Cardiac Hypertrophy." Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367757.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Griffith University. School of Medical Science.
Griffith Health
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Brenner, jacob Samuel. "Alternate routes of calcium entry mediating pathological cardiac hypertrophy /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Full textLoonat, Aminah Ahmed. "The involvement of p38 gamma MAPK in pathological cardiac hypertrophy." Thesis, King's College London (University of London), 2016. http://kclpure.kcl.ac.uk/portal/en/theses/the-involvement-of-p38gamma-mapk-in-pathological-cardiac-hypertrophy(f00e26a7-dab2-474d-9d3e-a52dfe9e873e).html.
Full textBarr, Larry A. "The Role of Calcium in the Regulation of Pathological Hypertrophy." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/254617.
Full textPh.D.
Pathological hypertrophy leads to cardiac dysfunction and heart failure. It is not clearly defined how this process occurs in the cardiomyocyte, or how the pathology can be effectively treated. There are numerous processes that lead to pathological hypertrophy. We developed two models to study pathological hypertrophy and the role that Ca2+ plays. In one model, we administered clinical doses of the leukemia therapeutic drug imatinib to neonatal ventricular cardiomyocytes. This drug has recently been found to be cardiotoxic, and we set out to understand if Ca2+ is involved. In the second model, we developed mice with overexpression of the Ca2+ entrance channel, the L-type calcium channel (LTCC), which leads to pathological hypertrophy over time. We instituted a chronic exercise regimen on these mice to learn if physiological hypertrophy can ameliorate detrimental aspects of pathological hypertrophy. After cardiomyocytes were treated with imatinib, they expressed enhanced Ca2+ activity. Levels of atrial natriuretic peptide (ANP) were up, signifying pathological hypertrophy. We determined that Ca2+ was activating Calcineurin, leading to translocation of nuclear factor of activated T-cells (NFAT) into the nucleus, resulting in hypertrophy. This activity was blocked by Ca2+ and Calcineurin inhibitors. We concluded that imatinib causes Ca2+ induced pathological hypertrophy. When mice with LTCC overexpression were exercised, they exhibited enhanced cardiac function. They also had thicker septal walls and increased chamber diameter, hallmarks of physiological hypertrophy. Heart weight to body weight ratio was significantly higher after exercise. When isolated hearts were administered ischemia/reperfusion injury, the exercised hearts showed a significant improvement in recovery compared to sedentary LTCC overexpressed hearts. Calcium activity was enhanced at the cardiomyocyte level in both mouse lines of exercised mice. In conclusion, hearts with a pathological hypertrophic phenotype can enhance function and achieve cardioprotection through chronic exercise.
Temple University--Theses
Harper, Shavonn Christine. "The Effects of Growth Differentiation Factor 11 on Pathological Cardiac Hypertrophy." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/498061.
Full textPh.D.
Pathological cardiac hypertrophy (PCH) occurs in response to pathological stimuli affecting the heart such as coronary artery disease, myocardial infarction, or hypertension. PCH is also be independent risk factor for cardiac events and/or sudden death. Despite therapeutic advancements in the treatment of cardiovascular diseases (CVD) and heart failure, deaths due to CVD remain the leading cause of mortality worldwide. Furthermore, treatment of these cardiovascular diseases slows their progression, but individuals eventually progress to heart failure, which has a 5-year survival rate of approximately 50 percent. There is a clear need for development of new therapies that can reverse PCH and the associated damage to the heart. As healthcare improves, populations are living longer, and illness due to age increases. One issue that occurs with aging is loss of normal cardiac function leading to heart failure. This functional decline is accompanied by morphological changes in the heart, including hypertrophy. Although it is well documented that myocardial remodeling occurs with aging, the mechanisms underlying these changes are poorly understood. Growth differentiation factor 11 (GDF11) is a member of the transforming growth factor β (TGF-β) superfamily of proteins, which regulate a number of cellular processes. Shared circulation of a young mouse with an old mouse or a single daily intraperitoneal (IP) injection of GDF11 for 30 days was shown to reverse aging-induced pathological cardiac hypertrophy. This molecule is highly homologous with another TGF-β family member, myostatin, which is a known negative growth regulator of skeletal muscle. We began by attempting to validate published data claiming that a single daily intraperitoneal (IP) injection of 0.1 mg/kg/day of GDF11 could reverse aging induced cardiac hypertrophy. We performed a blinded study during which treated 24-month-old C57BL/6 male mice with a single IP injection of 0.1 mg/kg/day of GDF11for 28 days and monitored changes in cardiac function and structure using echocardiography (ECHO). We also looked for differences in fibrosis, myocyte size, markers of pathological hypertrophy and heart weight. We were unable to find any differences between vehicle treated age mice and GDF11 treated aged mice in any of the measured parameters. While we did find an increase in heart weight between 8-week-old mice and the 24-month-old mice, there was no difference in the heart weight to body weight ratios of these groups of animals. From these data we concluded that our aged- mice did not have pathological hypertrophy and the dose of GDF11 used in this study did not have any effect on cardiac structure or function. Hypertensive heart disease results in changes in cardiac structure and function including left ventricular hypertrophy, systolic and/or diastolic dysfunction. It is also a leading cause of heart failure. Members of the TGF-β superfamily of proteins have been shown to be involved in many of the processes that occur in the heart in response to hypertension, such as the fibrotic response. Although it was previously shown that treatment with 0.1 mg/kg of GDF11 did not prevent pressure overload induced cardiac hypertrophy, we found this dose was too low to alter cardiac structure in our aging study. In addition, a single GDF11 dose is insufficient to fully address this issue. We therefore performed a blinded dose-ranging study to investigate the effects of GDF11 on pressure overload induced cardiac hypertrophy using transverse aortic constriction (TAC) which mimics the effects of chronic hypertension on the heart. In this study, animals received TAC surgery and were assigned to treatment groups so that there were no differences in wall thickness, cardiac function, or pressure gradients across the aortic constriction at the start of the treatments 1 week after TAC. Mice were given 0.5 mg/kg/day of GDF11, 1.0 mg/kg/day GDF11, 5.0 mg/kg/day of GDF11, or vehicle via a single daily IP injection for 14 days. Using these higher doses, we found that GDF11 had dose dependent effects on both cardiac structure and function following TAC. Myocyte cross sectional area was dose-dependently decreased compared to vehicle treated mice in both sham and TAC conditions. Cardiac function was preserved in the 1.0 and 5.0 mg/kg groups treatment groups after TAC. Left ventricular internal chamber dimensions were preserved with the 1.0 mg/kg treatment group. Treatment with GDF11 caused a dose dependent decrease on both body weight and heart weight in both normal and TAC mice, but with an effect on heart weight in the TAC mice that was independent of body weight. However, the 5.0 mg/kg dose caused large reductions in body weight (cachexia) and death. Our results show that GDF11 can reduce pathological hypertrophy and cardiac remodeling after pressure overload, but there is a narrow therapeutic range.
Temple University--Theses
Sculthorpe, Nicholas. "Left ventricular long axis dynamics in pathological and physiological left ventricular hypertrophy." Thesis, University of South Wales, 2002. https://pure.southwales.ac.uk/en/studentthesis/left-ventricular-long-axis-dynamics-in-pathological-and-physiological-left-ventricular-hypertrophy(eeeb9f18-b0d5-433b-b261-2907df223717).html.
Full textMakarewich, Catherine Anne. "MICRODOMAIN BASED CALCIUM INFLUX PATHWAYS THAT REGULATE PATHOLOGICAL CARDIAC HYPERTROPHY AND CONTRACTILITY." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/266828.
Full textPh.D.
Pathological cardiac stressors, including persistent hypertension or damage from ischemic heart disease, induce a chronic demand for enhanced contractile performance of the heart. The cytosolic calcium (Ca2+) transient that regulates myocyte contraction must be persistently increased in disease states in order to maintain cardiac output to sustain the metabolic requirements of the body. Associated with this enhanced intracellular Ca2+ ([Ca2+]i) state is pathological cardiac myocyte hypertrophy, which results in large part from the activation of Ca2+-dependent activation of calcineurin (Cn)-nuclear factor of activated T cells (NFAT) signaling. The puzzling feature of this hypertrophic signaling is that the cytosolic [Ca2+] that controls contractility appears to be separate from the [Ca2+] which activates Cn-NFAT signaling. The overarching theme of this dissertation is to explore the source and spatial constraints of pathological hypertrophic signaling Ca2+ and to investigate how it is possible that sensitive and finely tuned Ca2+-dependent signaling pathways are regulated in the background of massive Ca2+ fluctuations that oscillate between 100nM and upwards of 1-2μM during each cardiac contractile cycle. L-type Ca2+ channels (LTCCs) are a major source of Ca2+ entry in cardiac myocytes and are known to play an integral role in the initiation of myocyte excitation contraction-coupling (EC-coupling). We performed a number of experiments to show that a small population of LTCCs reside outside of EC-coupling domains within caveolin (Cav-3) signaling microdomains where they provide a local source of Ca2+ to activate Cn-NFAT signaling. We designed a Cav-targeted LTCC blocker that could eliminate Cn-NFAT activation but did not reduce myocyte contractility. The activity of Cav-targeted LTCCs could also be upregulated to enhance hypertrophic signaling without affecting contractility. Therefore, we believe that caveolae-localized LTCCs do not participate in EC-coupling, but instead act locally to control the coordinated activation of Cn-NFAT signaling that drives pathological remodeling. Transient Receptor Potential (TRP) channels are also thought to provide a source of Ca2+ for activation of hypertrophic signaling. The canonical family of TRP channels (TRPC) is expressed at low levels in normal adult cardiac tissue, but these channels are upregulated in disease conditions which implicates them as stress response molecules that could potentially provide a platform for hypertrophic Ca2+ signaling. We show evidence that TRPC channel abundance and function increases in cardiac stress conditions, such as myocardial infarction (MI), and that these channels are associated with hypertrophic responses, likely through a Ca2+ microdomain effect. While we found that TRPC channels housed in caveolae membrane microdomains provides a source of [Ca2+] for induction of cardiac hypertrophy, this effect also requires interplay with LTCCs. We also found that TRPC channels have negative effects on cardiac contractility, which we believe are due to local activation of Ca2+/calmodulin-dependent protein kinase (CaMKII) and subsequent modulation of ryanodine receptors (RyRs). Further, we found that inhibiting TRPC channels in a mouse model of MI led to increased basal myocyte contractility and reduced hypertrophy and cardiac structural and functional remodeling, as well as increased survival. Collectively, the data presented in this dissertation provides comprehensive evidence that Ca2+ regulation of Cn-NFAT signaling and resultant pathological hypertrophy can be coordinated by spatially localized and regulated Ca2+ channels. The compartmentalization of LTCCs and TRPC channels in caveolae membrane microdomains along with pathological hypertrophy signaling effectors makes for an attractive explanation for how Ca2+-dependent signaling pathways are regulated under conditions of continual Ca2+ transients that mediate cardiac contraction during each heart beat. Elucidation of additional Ca2+ signaling microdomains in adult cardiac myocytes will be important in more comprehensively resolving how myocytes differentiate between signaling versus contractile Ca2+.
Temple University--Theses
Assrafally, Farryah. "Modulation of pathological cardiac hypertrophy via the interleukin-10 signalling in the cardiomyocytes." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/modulation-of-pathological-cardiac-hypertrophy-via-the-interleukin10-signalling-in-the-cardiomyocytes(430247dd-1512-4e29-9f7a-288bae85fffd).html.
Full textBooks on the topic "Pathological hypertrophy"
D’Andrea, Antonello, André La Gerche, and Christine Selton-Suty. Systemic disease and other conditions: athlete’s heart. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0055.
Full textKaratasakis, G., and G. D. Athanassopoulos. Cardiomyopathies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0019.
Full textKjaer, Michael, and Abigail Mackey. Muscle. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199533909.003.0002.
Full textC Diaz, Eva, Celeste C Finnerty, and David N. Herndon. Severe Burn Injuries and Their Long-Term Implications. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0016.
Full textWyatt, Laura A., and Michael Doherty. Morphological aspects of pathology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0003.
Full textShirodaria, Cheerag, and Sam Dawkins. Chronic stable angina. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0089.
Full textBook chapters on the topic "Pathological hypertrophy"
Baker, Julien S., Fergal Grace, Lon Kilgore, David J. Smith, Stephen R. Norris, Andrew W. Gardner, Robert Ringseis, et al. "Pathological Cardiac Hypertrophy." In Encyclopedia of Exercise Medicine in Health and Disease, 690. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2841.
Full textKalmar, Jayne M., Brigid M. Lynch, Christine M. Friedenreich, Lee W. Jones, A. N. Bosch, Alessandro Blandino, Elisabetta Toso, et al. "Cardiac Hypertrophy, Pathological." In Encyclopedia of Exercise Medicine in Health and Disease, 168–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_38.
Full textCuspidi, Cesare, Laura Lonati, Lorena Sampieri, Gastone Leonetti, and Alberto Zanchetti. "Physiological Versus Pathological Hypertrophy." In Advances in Experimental Medicine and Biology, 145–58. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5385-4_16.
Full textJacob, R., M. Vogt, and H. Rupp. "Physiological and Pathological Hypertrophy." In Developments in Cardiovascular Medicine, 39–56. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2051-7_2.
Full textPluim, B. M., A. van der Laarse, and E. E. van der Wall. "The Athlete’s Heart: A Physiological or a Pathological Phenomenon?" In Left Ventricular Hypertrophy, 85–106. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_7.
Full textKato, Takao. "Genome Editing and Pathological Cardiac Hypertrophy." In Advances in Experimental Medicine and Biology, 87–101. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-5642-3_6.
Full textHe, Jianfeng, Yanhong Luo, Junxia Song, Tao Tan, and Hua Zhu. "Non-coding RNAs and Pathological Cardiac Hypertrophy." In Advances in Experimental Medicine and Biology, 231–45. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1671-9_13.
Full textOrellana, Juan, and Alan H. Friedman. "Congenital Hypertrophy of the Retinal Pigment Epithelium." In Clinico-Pathological Atlas of Congenital Fundus Disorders, 153–55. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9320-7_34.
Full textKolwicz, Stephen C., and Rong Tian. "Fuel Metabolism Plasticity in Pathological Cardiac Hypertrophy and Failure." In Cardiac Energy Metabolism in Health and Disease, 169–82. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1227-8_11.
Full textMerello, Giacomo, Luna Cavigli, and Flavio D’Ascenzi. "Physiological Versus Pathological Left Ventricular Hypertrophy in the Hypertensive Athlete." In Exercise, Sports and Hypertension, 101–11. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07958-0_7.
Full textConference papers on the topic "Pathological hypertrophy"
Hyekyeong Kwon, Jang-Soo Chun, Zee-Yong Park, and Dong-Yu Kim. "Poster title (mass spectrometric protein profiling analyses of pathological and physiological hypertrophy cardiac muscle tissues)." In 2012 IEEE 2nd International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2012. http://dx.doi.org/10.1109/iccabs.2012.6182652.
Full textRoby, Tiffany S., and Jiro Nagatomi. "Effect of Stretch on Bladder Smooth Muscle Cells in Three-Dimensional Culture." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176611.
Full textNavitsky, Michael A., Steven Deutsch, and Keefe B. Manning. "A Comparison of Thrombus Susceptibility for Two Pulsatile 50 CC Left Ventricular Assist Pumps." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80570.
Full textDolensky, Joseph R., Lauren D. C. Casa, and Ajit P. Yoganathan. "The Effect of Pulmonary Hypertension on Tricuspid Valve Coaptation in Normal and Pathologic Valve Geometries: An In Vitro Study." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80184.
Full textBaicu, Catalin F., and Michael R. Zile. "Quantification of Diastolic Viscoelastic Properties of Isolated Cardiac Muscle Cells." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23158.
Full textAgouni, Abdelali, Duck Y. Lee, Assaad A. Eid, Yves Gorin, and Kumar Sharma. "The Protective Role of Sestrin2 in High Fat Diet-Induced Nephropathy." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0134.
Full textRizzuto, E., A. Musarò, A. Catizone, and Z. Del Prete. "Morpho-Functional Interaction Between Muscle and Tendon in Hypertrophic MLC/mIGF-1 Mice." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19332.
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