Journal articles on the topic 'Clinical atherosclerosi'
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1
Momtazi-Borojeni, Amir Abbas, Sarvenaz Sabouri-Rad, Antonio M. Gotto, Matteo Pirro, Maciej Banach, Zuhier Awan, George E. Barreto, and Amirhossein Sahebkar. "PCSK9 and inflammation: a review of experimental and clinical evidence." European Heart Journal - Cardiovascular Pharmacotherapy 5, no. 4 (June 25, 2019): 237–45. http://dx.doi.org/10.1093/ehjcvp/pvz022.
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AbstractProprotein convertase subtilisin/kexin Type 9 (PCSK9) is now identified as an important and major player in hypercholesterolaemia and atherosclerosis pathophysiology. PCSK9, through promoting lysosomal degradation of hepatic low-density lipoprotein (LDL) receptor, can decrease the clearance of plasma LDLs, leading to hypercholesterolaemia and consequent atherosclerotic plaque formation. Hypercholesterolaemia has been found to promote systemic and vascular inflammation, which can cause atherosclerotic lesion formation and progression and subsequent incidence of cardiovascular disease. Recent studies have shown the involvement of PCSK9 in the inflammatory pathway of atherosclerosis. Although trials with PCSK9 inhibitors have not shown any alteration in plasma C-reactive protein levels, there is accumulating evidence showing lessened inflammatory response in the arterial wall that could attenuate atherosclerotic plaque development beyond the established LDL-lowering effect of PCSK9 inhibition. In this review, we represent mounting evidence indicating that PCSK9 can locally increase vascular inflammation and contribute to atherosclerotic plaque progression in patients with hypercholesterolaemia.
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Millon, Antoine, Emmanuelle Canet-Soulas, Loic Boussel, Zahi Fayad, and Philippe Douek. "Animal models of atherosclerosis and magnetic resonance imaging for monitoring plaque progression." Vascular 22, no. 3 (June 2014): 221–37. http://dx.doi.org/10.1177/1708538113478758.
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Atherosclerosis, the main cause of heart attack and stroke, is the leading cause of death in most modern countries. Preventing clinical events depends on a better understanding of the mechanism of atherosclerotic plaque destabilization. Our knowledge on the characteristics of vulnerable plaques in humans has grown past decades. Histological studies have provided a precise definition of high-risk lesions and novel imaging methods for human atherosclerotic plaque characterization have made significant progress. However the pathological mechanisms leading from stable lesions to the formation of vulnerable plaques remain uncertain and the related clinical events are unpredictable. An animal model mimicking human plaque destablization is required as well as an in vivo imaging method to assess and monitor atherosclerosis progression. Magnetic resonance imaging (MRI) is increasingly used for in vivo assessment of atherosclerotic plaques in the human carotids. MRI provides well-characterized morphological and functional features of human atherosclerotic plaque which can be also assessed in animal models. This review summarizes the most common species used as animal models for experimental atherosclerosis, the techniques to induce atherosclerosis and to obtain vulnerable plaques, together with the role of MRI for monitoring atherosclerotic plaques in animals.
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Shramko, V. S., S. V. Morozov, E. I. Chernyak, L. V. Shcherbakova, A. V. Kurguzov, A. M. Chernyavskyi, and Yu I. Ragino. "Clinical characteristics of patients with coronary atherosclerosis depending on blood fatty acids." Complex Issues of Cardiovascular Diseases 9, no. 1 (March 25, 2020): 15–24. http://dx.doi.org/10.17802/2306-1278-2020-9-1-15-24.
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Aim. To examine the differences in clinical parameters in patients with coronary atherosclerosis based on fatty acid profile.Methods.60 men with angiographically verified atherosclerosis of the coronary arteries underwent the analysis of fatty acids followed by coronary endarterectomy. Patients were divided into two groups after histological analysis of the intimamedia fragments. Men without unstable plaques in the coronary arteries were included in Group 1, whereas patients with unstable atherosclerotic plaques were included in Group 2. Blood serum levels of fatty acids were measured by highefficiency gas-liquid chromatography.Results.The predicted probability value and the predicted group membership in men with coronary atherosclerosis were calculated using the logistic regression. The following clinical patterns in men with unstable atherosclerotic plaques included increased prevalence of myocardial infarction with the event over 10 years ago, severe angina pectoris (III and IV functional class) and chronic heart failure, in comparison with CAD patients without unstable plaques.Conclusion. Fatty acid profile was associated with altered individual history of coronary atherosclerosis.
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Lee, Cadence F., Rachel E. Carley, Celia A. Butler, and Alan R. Morrison. "Rac GTPase Signaling in Immune-Mediated Mechanisms of Atherosclerosis." Cells 10, no. 11 (October 20, 2021): 2808. http://dx.doi.org/10.3390/cells10112808.
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Coronary artery disease caused by atherosclerosis is a major cause of morbidity and mortality around the world. Data from preclinical and clinical studies support the belief that atherosclerosis is an inflammatory disease that is mediated by innate and adaptive immune signaling mechanisms. This review sought to highlight the role of Rac-mediated inflammatory signaling in the mechanisms driving atherosclerotic calcification. In addition, current clinical treatment strategies that are related to targeting hypercholesterolemia as a critical risk factor for atherosclerotic vascular disease are addressed in relation to the effects on Rac immune signaling and the implications for the future of targeting immune responses in the treatment of calcific atherosclerosis.
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Song, Boce, Yulong Bie, Haoxin Feng, Beili Xie, Mingwang Liu, and Fuhai Zhao. "Inflammatory factors driving atherosclerotic plaque progression new insights." Journal of Translational Internal Medicine 10, no. 1 (March 1, 2022): 36–47. http://dx.doi.org/10.2478/jtim-2022-0012.
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Abstract Coronary atherosclerosis is a chronic inflammatory disease that can lead to varying degrees of blood flow obstruction and a common pathophysiological basis of cardiovascular disease. Inflammatory factors run through the whole process of atherosclerotic lesions. Macrophages, T cells, and neutrophils play important roles in the process of atherosclerotic inflammation. Considering the evolutionary characteristics, atherosclerosis can be divided into different stages as early atherosclerotic plaque, plaque formation stage, and plaque rupture stage. In this paper, the changes in inflammatory cells at different stages of lesions and their related mechanisms are discussed, which can provide new insights from a clinical to bench perspective for atherosclerosis me chanism.
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Bjelajac, Aleksandra, Alvin KY Goo, and C. Wayne Weart. "Prevention and Regression of Atherosclerosis: Effects of Hmg-CoA Reductase Inhibitors." Annals of Pharmacotherapy 30, no. 11 (November 1996): 1304–15. http://dx.doi.org/10.1177/106002809603001116.
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OBJECTIVE: TO review the current literature on the effects of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors in secondary prevention and regression of atherosclerosis. DATA SOURCES A MEDLINE and journal search of recent studies evaluating the effects of lipid lowering with HMG-CoA reductase inhibitors on serum cholesterol as well as progression and regression of atherosclerotic coronary or carotid disease in patients with established atherosclerotic disease was conducted. Articles addressing the pathophysiology of atherosclerotic disease were identified by using the same sources. STUDY SELECTION: All available studies evaluating the use of HMG-CoA reductase inhibitors in the progression and regression of coronary and carotid atherosclerosis were reviewed. DATA SYNTHESIS: Lowering of total serum cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increasing high-density lipoprotein cholesterol can be achieved with HMG-CoA reductase inhibitors. Aggressive lipid lowering has been demonstrated to alter progression of established atherosclerotic disease and, in some patients, actually induce regression of the atheroma. An unexpected finding of several trials was the early and significant reduction in clinical cardiac events. Other mechanisms by which clinical event reduction may be explained include plaque stabilization and restoration of endothelium vasodilation. CONCLUSIONS: Aggressive lipid-lowering therapy using HMG-CoA reductase inhibitors appears to alter the natural progression and promote regression of atherosclerosis in selected patients with established coronary or carotid atherosclerosis. However, it is unlikely that regression of atherosclerosis alone is responsible for the marked reduction in clinical cardiac events seen in these trials.
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Poredoš, Pavel, and Mateja Kaja Ježovnik. "Markers of preclinical atherosclerosis and their clinical relevance." Vasa 44, no. 4 (July 2015): 247–56. http://dx.doi.org/10.1024/0301-1526/a000439.
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Abstract. The estimation of risk for atherosclerotic and cardiovascular events based only on the presence of classical risk factors is often insufficient. Therefore, efforts have been made to find markers that indicate the presence of preclinical disease in individual subjects: blood markers of atherosclerosis and preclinical deterioration of the arterial wall. Elevated levels of several inflammatory mediators have been found in subjects with atherosclerosis. Increased basal levels of cytokines, the cell adhesion molecules, selectins and acute-phase reactants such as high sensitive C-reactive protein (hsCRP), fibrinogen, and serum amyloid A are related to an increased risk of cardiovascular events. For clinical purposes, the most promising inflammatory biomarker appears to be hsCRP. In the last decade, markers of plaque stability and unstable coronary artery disease have been sought. Further, markers of endothelial dysfunction, like circulating molecules as well as indicators of functional deterioration of the arterial wall were identified. It was shown that endothelial dysfunction is closely related to different risk factors of atherosclerosis, and to their intensity and duration. Intima-media thickness measurement has emerged as one of the methods of choice for determining the anatomic extent of preclinical atherosclerosis and for assessing cardiovascular risk.Determination of markers of preclinical atherosclerosis improve individual risk determination and could influence the decision of a clinician to intervene with medication and to use more aggressive treatment of risk factors in high risk subjects and in patients with atherosclerotic disease.
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Babintseva, Yanina D., A. M. Sergeeva, V. P. Karagodin, and A. N. Orekhov. "Atherogenesis in human - clinical aspects of circulating immune complexes." Clinical Medicine (Russian Journal) 94, no. 5 (June 20, 2016): 325–32. http://dx.doi.org/10.18821/0023-2149-2016-94-5-325-332.
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It has been suggested that circulating immune complexes containing low density lipoproteins (LDL-CIC) play a role in atherogenesis and are involved in the formation of early atherosclerotic lesions. The complexes, as well as anti-LDL antibody were found in the blood of patients with atherosclerotic process in various cardiovascular diseases, well as in the blood of animals with experimentally modulated atherosclerosis. One can assume that the presence anti-LDL antibodies in blood is a result of an immune response that is induced by modification of lipoproteins. LDL-CIC differ from native LDL in many aspects. They have much lower levels of sialic acid, a smaller diameter and a higher density electronegativity than native LDL. The fraction of the LDL-CIC in serum is an important manifestation of the atherosclerotic process. LDL-CIC, unlike the native LDL is able to induce intracellular accumulation of neutral lipids, especially esterified cholesterol in cell cultures obtained from healthy human aortic intima and macrophages in culture. After removal of the LDL-CIC, the serum of CHD-patients loses its atherogenic properties. The titer of the LDL-CIC in the blood serum significantly correlate with the progression of atherosclerosis and in vivo has the highest diagnostic yield of measured among other lipid parameters. Increasing CIC- cholesterol could also increase the risk of coronary artery atherosclerosis.
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Tu, Shuangshuang, Wenming He, Jinru Han, Aiguo Wu, and Wenzhi Ren. "Advances in imaging and treatment of atherosclerosis based on organic nanoparticles." APL Bioengineering 6, no. 4 (December 1, 2022): 041501. http://dx.doi.org/10.1063/5.0127835.
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Atherosclerosis, a systemic chronic inflammatory disease, can lead to thrombosis and vascular occlusion, thereby inducing a series of serious vascular diseases. Currently, distinguishing unstable plaques early and achieving more effective treatment are the two main clinical concerns in atherosclerosis. Organic nanoparticles have great potential in atherosclerotic imaging and treatment, showing superior biocompatibility, drug-loading capacity, and synthesis. This article illustrates the process of atherosclerosis onset and the key targeted cells, then systematically summarizes recent progress made in organic nanoparticle-based imaging of different types of targeted cells and therapeutic methods for atherosclerosis, including optical and acoustic-induced therapy, drug delivery, gene therapy, and immunotherapy. Finally, we discuss the major impediments that need to be addressed in future clinical practice. We believe this article will help readers to develop a comprehensive and in-depth understanding of organic nanoparticle-based atherosclerotic imaging and treatment, thus advancing further development of anti-atherosclerosis therapies.
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Pakzad, Bahram, Elham Rajae, Saeid Shahrabi, Somayeh Mansournezhad, Nader Davari, Shirin Azizidoost, and Najmaldin Saki. "T-Cell Molecular Modulation Responses in Atherosclerosis Anergy." Laboratory Medicine 51, no. 6 (February 27, 2020): 557–65. http://dx.doi.org/10.1093/labmed/lmaa003.
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Abstract Atherosclerosis continues to be a major cause of death in patients with cardiovascular diseases. The cooperative role of immunity has been recently considered in atherosclerotic plaque inflammation, especially adaptive immune response by T cells. In this review, we examine the possible role of T cells in atherosclerosis-mediated inflammation and conceivable therapeutic strategies that can ameliorate complications of atherosclerosis. The cytokines secreted by T-lymphocyte subsets, different pathophysiological profiles of microRNAs (miRs), and the growth factor/receptor axis have diverse effects on the inflammatory cycle of atherosclerosis. Manipulation of miRNA expression and prominent growth factor receptors involved in inflammatory cytokine secretion in atherosclerosis can be considered diagnostic biomarkers in the induction of anergy and blockade of atherosclerotic development. This manuscript reviews immunomodulation of T cells responses in atherosclerosis anergy.
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Svyrydova, N. K., O. V. Popov, N. O. Kravchuk, N. l. Ingula, A. S. Bondarenko, K. M. Usovych, V. Y. Svystun, and B. V. Lytvychenko. "The condition of the acute cerebral circulation for the ischemic type: the clinical case." East European Journal of Neurology, no. 5(5) (September 20, 2015): 9–12. http://dx.doi.org/10.33444/2411-5797.2015.5(5).9-12.
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Cardiovascular diseases (COD] occupy a leading place in the structure of general morbidity, primary disability and total mortality in Ukraine. Atherosclerosis is a systemic disease of the large and medium-sized arteries causing luminal narrowing (focal or diffuse) as a result of the accumulation of lipid and fibrous material between the intimal and medial layers of the vessel. Atherosclerosis involves an ongoing inflammatory response. Atherosclerosis leads to the formation of atherosclerotic plaques, which gradually increases in size and narrows the lumen of the vessel. Hypertension and atherosclerosis are the most common of the studied risk factors that lead to the development of stroke.
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Magaeva, S. V., A. A. Kubatiev, E. A. Shirokov, and V. B. Simonenko. "Regression of atherosclecrotic lesions: medicinal and alimentary factors." Clinical Medicine (Russian Journal) 94, no. 9 (November 2, 2016): 668–71. http://dx.doi.org/10.18821/0023-2149-2016-94-9-668-671.
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The article reports results of clinical studies aimed to elucidate the influence of medicines on the size and density of atherosclerotic plaques in the walls of coronary and cerebral arteries. The phenomenon of regression of atherosclerotic lesions in the survivors of Leningrad siege during a long period of starvation is analyzed. The influence of inhibitors of angiotensinconverting enzyme on apoptosis of smooth muscle and foam cells of atherosclerotic plaques in the sanological mechanisms of atherosclerosis is discussed. The concept of natural regression of atherosclerosis is formulated and the necessity of development of the methods for is pharmacological activation are formulated.
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Marchini, Timoteo, Tijani Abogunloko, and Dennis Wolf. "Modulating Autoimmunity against LDL: Development of a Vaccine against Atherosclerosis." Hämostaseologie 41, no. 06 (December 2021): 447–57. http://dx.doi.org/10.1055/a-1661-1908.
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AbstractAtherosclerosis is a chronic inflammatory disease of the arterial wall that leads to the build-up of occluding atherosclerotic plaques. Its clinical sequelae, myocardial infarction and stroke, represent the most frequent causes of death worldwide. Atherosclerosis is a multifactorial pathology that involves traditional risk factors and chronic low-grade inflammation in the atherosclerotic plaque and systemically. This process is accompanied by a strong autoimmune response that involves autoreactive T cells in lymph nodes and atherosclerotic plaques, as well as autoantibodies that recognize low-density lipoprotein (LDL) and its main protein component apolipoprotein B (ApoB). In the past 60 years, numerous preclinical observations have suggested that immunomodulatory vaccination with LDL, ApoB, or its peptides has the potential to specifically dampen autoimmunity, enhance tolerance to atherosclerosis-specific antigens, and protect from experimental atherosclerosis in mouse models. Here, we summarize and discuss mechanisms, challenges, and therapeutic opportunities of immunomodulatory vaccination and other strategies to enhance protective immunity in atherosclerosis.
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Poels, Kikkie, Suzanne I. M. Neppelenbroek, Marie José Kersten, M. Louisa Antoni, Esther Lutgens, and Tom T. P. Seijkens. "Immune checkpoint inhibitor treatment and atherosclerotic cardiovascular disease: an emerging clinical problem." Journal for ImmunoTherapy of Cancer 9, no. 6 (June 2021): e002916. http://dx.doi.org/10.1136/jitc-2021-002916.
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Antibody-mediated blockade of co-inhibitory molecules such as cytotoxic T lymphocyte-associated protein 4, PD1 and PDL1 elicits potent antitumor responses and improves the prognosis of many patients with cancer. As these immune checkpoint inhibitors (ICIs) are increasingly prescribed to a diverse patient population, a broad range of adverse effects is emerging. Atherosclerosis, a lipid-driven chronic inflammatory disease of the large arteries, may be aggravated by ICI treatment. In this review, we discuss recent clinical studies that analyze the correlation between ICI use and atherosclerotic cardiovascular disease (CVD). Indeed, several studies report an increased incidence of atherosclerotic CVD after ICI administration, with the occurrence of pathologies such as myocardial infarction, ischemic stroke and coronary artery disease significantly higher after ICI use. Increased awareness and better monitoring of ICI-treated patients can elucidate risk factors that contribute to ICI-induced aggravation of atherosclerosis and identify promising treatment strategies. For now, optimal cardiovascular risk assessment is required to protect ICI-receiving patients and long-term survivors of cancer from the detrimental effects of ICI therapy on atherosclerotic CVD.
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Jednacz, Ewa, and Lidia Rutkowska-Sak. "Atherosclerosis in Juvenile Idiopathic Arthritis." Mediators of Inflammation 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/714732.
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Atherosclerosis is a chronic inflammatory disease of the arteries. Clinical consequences of the atherosclerotic process occur in the adult population, however atherosclerotic process begins in childhood. The classic risk factors for atherosclerosis include obesity, dyslipidaemia, age, gender or family history. In recent years, attention has been drawn to the similarity between atherosclerotic inflammatory processes and inflammatory changes in the course of systemic connective tissue disease, in particular systemic lupus etythematosus (SLE) or rheumatoid arthritis (RA). There is also observed the similarity of the pathogenetic background of development of atherosclerosis and juvenile idiopathic arthritis (JIA). Elevated levels of pro-inflammatory cytokines are observed in the course of juvenile idiopathic arthritis. Also homocysteine concentrations, which may play a significant role in the development of atherosclerotic lesions, are observed higher in patients with JIA. Some studies revealed higher carotid intima-media thickness (IMT) index values in children with JIA. In view of the fact that atherosclerotic process begins as early as in childhood, the introduction of appropriate preventive measures in children is a matter of utmost importance.
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Kuznetsova, Alla, Anastasiya Dolgushina, Albina Savochkina, Lubov Pykhova, Veronika Sumerkina, Anna Selyanina, Yana Kudrinskaya, and Vadim Genkel. "Liver Stiffness Is Associated with the Burden of Carotid and Systemic Atherosclerosis in an Unorganized Cohort of Patients 40–64 Years Old." Diagnostics 12, no. 10 (September 27, 2022): 2336. http://dx.doi.org/10.3390/diagnostics12102336.
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Background: The aim of the study is to research the relationship between the severity of liver fibrosis and the burden of carotid and systemic atherosclerosis. Methods: The study includes 163 patients 40 to 64 years of age without atherosclerotic CVD or liver disease. All patients underwent duplex scanning of the carotid and lower limb arteries. All patients underwent transient liver elastometry using the FibroScan (Echosens, France). Results: Carotid plaque was detected in 110 (67.5%) patients. Based on the results of linear regression analysis, relationships between liver stiffness and carotid total plaque area (r = 0.21; p = 0.025) were found. Significant relationships were established between liver stiffness and atherosclerosis burden score based on the results of linear regression (r = 0.17; p = 0.029). Liver stiffness showed moderate diagnostic performance (AUC 0.666; p = 0.01) with regard to generalized atherosclerosis. An increase in liver stiffness >4.5 kPa was associated with an odds ratio of generalized atherosclerosis of 3.48 (95% CI 1.07–11.3; p = 0.038) after adjusting confounding factors. Conclusion: Among patients 40–64 years of age without established atherosclerotic CVD and liver disease, liver stiffness directly correlates with the burden of carotid and systemic atherosclerosis. Liver stiffness showed moderate diagnostic performance (AUC 0.666; p = 0.01) with regard to generalized atherosclerosis.
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Liu, Ke, Bangzhu Chen, Fanwen Zeng, Gang Wang, Xin Wu, Yueshu Liu, Guiling Li, Jiarong Yan, and Shouquan Zhang. "ApoE/NOS3 Knockout Mice as a Novel Cardiovascular Disease Model of Hypertension and Atherosclerosis." Genes 13, no. 11 (November 1, 2022): 1998. http://dx.doi.org/10.3390/genes13111998.
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Hypertension is an independent risk factor for atherosclerosis. However, few models of hypertensive atherosclerosis have been established in medical research. In this study, we crossed the ApoE knockout (ApoE-KO; ApoE−/−) atherosclerotic mouse model with the NOS3 knockout (NOS3-KO; NOS3−/−) hypertensive mouse model to establish an ApoE/NOS3 double knockout (ApoE/NOS3-KO; ApoE/NOS3−/−) hypertensive atherosclerosis mouse model. We found that ApoE/NOS3−/− mice reproduced normally, had a blood pressure of 133.00 ± 3.85 mmHg, and developed hypertensive fundus retinopathy and hypertensive nephropathy. In addition, serum total cholesterol (TC) and low-density lipoprotein (LDL) levels in the blood were abnormally elevated, steatosis was observed in the liver cells, and atherosclerotic lesions were observed in the aortic vessels in ApoE/NOS3−/− adult mice. In conclusion, ApoE/NOS3−/− adult mice are a satisfactory model of hypertension and atherosclerosis and can be utilized for studies on cardiovascular diseases.
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Burnett, John R., and Samuel D. Vasikaran. "Cardiovascular disease and osteoporosis: is there a link between lipids and bone?" Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 39, no. 3 (May 1, 2002): 203–10. http://dx.doi.org/10.1258/0004563021902134.
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Atherosclerotic heart disease and osteoporosis are both diseases of old age. Evidence is accumulating for a link between vascular and bone disease. Calcification is a common feature of atherosclerotic plaques, and osteoporosis is associated with both atherosclerosis and vascular calcification. However, the relationship of vascular calcification to the pathogenesis of atherosclerosis remains incompletely understood. Hormone replacement therapy has beneficial effects in the prevention of both atherosclerosis and osteoporosis. Bisphosphonates inhibit bone resorption and are used in the treatment of osteoporosis, whereas the statins inhibit cholesterol biosynthesis and are used for the treatment of atherosclerosis. We have reviewed recent advances in the knowledge of the actions of bisphosphonates and statins at the cellular, molecular and end-organ levels in order to examine the relationship between cardiovascular disease and osteoporosis and to explore the link between lipids and bones. These studies suggest that the mechanism of actions of these two classes of drugs at the cellular level may not be mutually exclusive. There are some early clinical data to complement these findings, suggesting that statins increase bone density and bisphosphonates may have a beneficial effect in vivo on plasma lipid levels and on the atherosclerotic process. Properly designed prospective studies that examine the effect of statins on bone density and fractures, as well as the effects of bisphosphonates on lipid profiles, atherosclerotic progression and cardiovascular morbidity and mortality are needed to define clearly the clinical effects and potential new roles for these agents.
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Aengevaeren, Vincent L., Arend Mosterd, Sanjay Sharma, Niek H. J. Prakken, Stefan Möhlenkamp, Paul D. Thompson, Birgitta K. Velthuis, and Thijs M. H. Eijsvogels. "Exercise and Coronary Atherosclerosis." Circulation 141, no. 16 (April 21, 2020): 1338–50. http://dx.doi.org/10.1161/circulationaha.119.044467.
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Physical activity and exercise training are effective strategies for reducing the risk of cardiovascular events, but multiple studies have reported an increased prevalence of coronary atherosclerosis, usually measured as coronary artery calcification, among athletes who are middle-aged and older. Our review of the medical literature demonstrates that the prevalence of coronary artery calcification and atherosclerotic plaques, which are strong predictors for future cardiovascular morbidity and mortality, was higher in athletes compared with controls, and was higher in the most active athletes compared with less active athletes. However, analysis of plaque morphology revealed fewer mixed plaques and more often only calcified plaques among athletes, suggesting a more benign composition of atherosclerotic plaques. This review describes the effects of physical activity and exercise training on coronary atherosclerosis in athletes who are middle-aged and older and aims to contribute to the understanding of the potential adverse effects of the highest doses of exercise training on the coronary arteries. For this purpose, we will review the association between exercise and coronary atherosclerosis measured using computed tomography, discuss the potential underlying mechanisms for exercise-induced coronary atherosclerosis, determine the clinical relevance of coronary atherosclerosis in middle-aged athletes and describe strategies for the clinical management of athletes with coronary atherosclerosis to guide physicians in clinical decision making and treatment of athletes with elevated coronary artery calcification scores.
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Drapkina, O. M., O. N. Korneeva, and N. V. Mankova. "Subclinical atherosclerosis: The benefits of calcium antagonists." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 18, no. 2 (April 28, 2012): 118–25. http://dx.doi.org/10.18705/1607-419x-2012-18-2-118-125.
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Recently the research has been focused on the earlier stages of the atherosclerotic process, i.e. subclinical atherosclerosis. Endothelial dysfunction is a suitable marker of subclinical atherosclerosis. In routine clinical practice, ultrasonography is the most useful and accessible non-invasive method for diagnosis of subclinical atherosclerosis. Carotid intimai media thickness (IMT) was shown to be predictive for the risk of cardiovascular events. Furthermore, vascular stiffness can be a helpful marker for assessment of the vascular wall state and blood flow. Calcium antagonists (CA) seem to be promising for the prevention of subclinical atherosclerosis progression, and amlodipine has the priority due to the metabolic neutralilty, vasodilation effect and favourable effects on renal hemodynamics. The data on IMT assessement showed that amlodipine slows down the development of atherosclerotic lesions in hypertensive patients.
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Saranchina, J. V., S. V. Dutova, O. Y. Kilina, N. V. Khanarin, and T. S. Kulakova. "Features of interleukin-19 production in patients with atherosclerosis." Siberian Journal of Clinical and Experimental Medicine 36, no. 2 (July 7, 2021): 52–60. http://dx.doi.org/10.29001/2073-8552-2021-36-2-52-60.
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Objective. To study the features of local and systemic production of interleukin-19 in patients with atherosclerosis.Material and Methods. The study comprised a total of 46 patients (26 women and 20 men) treated for arterial hypertension in the therapeutic department of Republican Clinical Hospital named after G.Y. Remishevskaya. The mean age of subjects was 63.4 ± 3.2 years. The control group included 40 patients (23 women and 17 men aged 44.7 ± 5.5 years) who did not have atherosclerosis. Samples of atherosclerotic plaques and venous blood were examined. Atherosclerotic plaques were obtained by endarterectomy and then subjected to homogenization followed by enzymatic hydrolysis for 1 h at 37 °C with collagenase IV in the presence of proteinase III inhibitors. The serum levels of cytokines (in the control group and in patients with atherosclerosis) and in the atherosclerotic plaque homogenate (in patients with atherosclerosis) were determined by ELISA. To assess the cytokine-producing capacity of blood leukocytes and white blood cells isolated from atherosclerotic plaques, spontaneous and phytohemagglutinin (PHA)-induced cytokine production was determined when the cells were cultured in RPMI-1640.Results. The serum levels of IL-19 did not significantly differ between the patients with atherosclerosis and the control group. A statistically significant two-fold increase in the spontaneous expression of IL-19 by blood leukocytes was observed in the group of patients with atherosclerosis in comparison with the control group. When comparing the contents of IL-19 in blood serum and atherosclerotic plaque homogenate in patients with atherosclerosis, no statistically significant differences were found (p = 0.182). The level of PHA-induced IL-19 production by the atherosclerotic plaque white blood cells was significantly lower than that of blood leucocytes.Conclusion. The study showed that the reserve capacity for IL-19 synthesis in the atherosclerotic plaque white blood cells decreases leading to the progression of inflammation. The obtained results suggest that IL-19 plays the anti-atherogenic role and its production is involved in the maintaining the mechanisms for down-regulation of inflammation in atherosclerotic plaques.
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Darmawan, Hardi. "Bridging Coronary Physiology into Clinical Application of Acute Coronary Syndrome." Arkus 5, no. 1 (October 26, 2021): 195–97. http://dx.doi.org/10.37275/arkus.v5i1.123.
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Normal arteries have three layers of structure, tunica intima, tunica media, and tunica adventitia. Intima tunica is the deepest layer of coronary arteries in which there are antithrombotic molecules such as heparin sulfate, thrombomodulin, and plasminogen activator. In addition, tunica intima also contains substances that regulate the contraction of tunica smooth muscle cell media, called nitric oxide (vasodilators) and prostacyclin (vasoconstrictors). Tunica intima and tunica media seem to be directly related to the atherosclerosis process. Meanwhile, the role of tunika adventisia is unknown. The accumulation of atherosclerotic lesions and hemodynamic stress factors and the degradation of extracellular matrix will cause susceptibility of atherosclerotic plaque fibrous capsules to rupture and form thrombus. Thrombus that occurs in the coronary condition causes acute coronary syndrome, characterized by typical symptoms such as chest pain depending on the thrombus formed. In studying acute coronary syndromes, of course it cannot be separated from understanding the physiology of coronary arteries and the process of atherosclerosis. Therefore, this article aims to briefly explain coronary physiology.
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Ząbczyk, Michał, Joanna Natorska, and Anetta Undas. "Fibrin Clot Properties in Atherosclerotic Vascular Disease: From Pathophysiology to Clinical Outcomes." Journal of Clinical Medicine 10, no. 13 (July 5, 2021): 2999. http://dx.doi.org/10.3390/jcm10132999.
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Fibrin is a major component of thrombi formed on the surface of atherosclerotic plaques. Fibrin accumulation as a consequence of local blood coagulation activation takes place inside atherosclerotic lesions and contributes to their growth. The imbalance between thrombin-mediated fibrin formation and fibrin degradation might enhance atherosclerosis in relation to inflammatory states reflected by increased fibrinogen concentrations, the key determinant of fibrin characteristics. There are large interindividual differences in fibrin clot structure and function measured in plasma-based assays and in purified fibrinogen-based systems. Several observational studies have demonstrated that subjects who tend to generate denser fibrin networks displaying impaired clot lysis are at an increased risk of developing advanced atherosclerosis and arterial thromboembolic events. Moreover, the majority of cardiovascular risk factors are also associated with unfavorably altered fibrin clot properties, with their improvement following effective therapy, in particular with aspirin, statins, and anticoagulant agents. The prothrombotic fibrin clot phenotype has been reported to have a predictive value in terms of myocardial infarction, ischemic stroke, and acute limb ischemia. This review article summarizes available data on the association of fibrin clot characteristics with atherosclerotic vascular disease and its potential practical implications.
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Lizunov, Aleksey V., and Evgenii R. Bychkov. "Molecular mechanisms of antiatherogenic drugs action." Reviews on Clinical Pharmacology and Drug Therapy 19, no. 3 (October 8, 2021): 291–301. http://dx.doi.org/10.17816/rcf193291-301.
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The purpose of this review is the analysis of the molecular mechanisms of lipid metabolism, their disorders leading to atherosclerosis, and the influence of modern antiatherogenic and antihyperlipidemic agents on atherogenic mechanisms. At the beginning of the review, a general description of atherosclerosis as pathology, its main characteristics and factors is given. The question of the complexity of the treatment of atherosclerosis and the problems arising in connection with the complexity is considered. Current models of the nature of atherosclerotic lesions are described. Next, we consider modern anti-atherosclerotic drugs used in clinical practice. Their nomenclature is given. Their basic biochemical mechanisms and the nature of their action are analyzed. Their negative effects and side effects are also considered. Then, the molecular and genetic mechanisms associated with atherosclerosis are analyzed in detail. The genes associated with lipid metabolism and the formation of atherosclerotic plaques, their expression and regulation are considered. The question of the influence of known anti-atherosclerotic agents on their expression is also covered. A group of azole drugs and their effect on lipid metabolism are considered in the context of the search for new anti-atherogenic drugs. The final part of the review examines the relevance of the search for new anti-atherosclerotic agents and methods for modeling dyslipidemia as a model of conditions that correlate with anti-atherosclerotic vascular lesions. It was concluded that the search for antiatherogenic drugs among imidazole derivatives is promising.
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Liu, Dekun, Yueyue Song, Tinging Song, Lin Lin, Lei Zhang, Qiong Yang, Xingchen Niu, et al. "RRP Regulates Autophagy through the AMPK Pathway to Alleviate the Effect of Cell Senescence on Atherosclerosis." Oxidative Medicine and Cellular Longevity 2023 (January 30, 2023): 1–22. http://dx.doi.org/10.1155/2023/9645789.
Full textAbstract:
Autophagy is closely associated with atherosclerosis and other cardiovascular diseases (CVD). Compound Danshen prescription is widely used as a clinical antiatherosclerotic drug. In our previous studies, we have shown that the combined active component, ginsenoside Rg1-notoginsenoside R1-protocatechualdehyde (RRP), can effectively alleviate endothelial dysfunction and reduce atherosclerotic plaques. However, the association between cellular senescence, caused by reduced autophagy, and atherosclerosis remains unclear. In this study, we investigated whether RRP can enhance autophagy and alleviate cell senescence through the AMPK pathway. Our results showed that RRP reduced the secretion of inflammatory factors in the serum of atherosclerotic mice, enhanced autophagy, and alleviated aortic aging in mice, thus reducing atherosclerotic plaques. In human aortic endothelial cells (HAECs), RRP effectively enhanced autophagy and inhibited senescence by activating the AMPK pathway. When AMPKα was silenced, the effect of RRP was inhibited, thus reversing its antiaging effect. Overall, our results show that RRP regulates autophagy through the AMPK pathway, thereby inhibiting cell senescence and alleviating the progression of atherosclerosis, suggesting that RRP may be a potential candidate drug for the treatment of atherosclerosis.
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Yaroslavskaya, E. I., V. A. Kuznetsov, E. A. Gorbatenko, and S. M. Dyachkov. "CALCULATOR OF NON-OBSTRUCTIVE CORONARY ATHEROSCLEROSIS: CLINICAL CASE OF A MALE PATIENT WITH SUSPECTED CORONARY ARTERY DISEASE." Siberian Medical Journal 33, no. 3 (November 28, 2018): 93–101. http://dx.doi.org/10.29001/2073-8552-2018-33-3-93-101.
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Evidence suggests that most myocardial infarctions result from ruptures of the atherosclerotic plaques that do not significantly compromise coronary lumen before the event. However, detection of nonsignificant coronary lesions in patients with suspected coronary artery disease without coronary angiography is challenging. We developed a calculator for nonobstructive coronary atherosclerosis based on patient gender, age, and the presence or absence of the echocardiographic signs of ascending aorta atherosclerosis and arterial hypertension. The calculator may be used for determining the probability of non-obstructive coronary atherosclerosis and for promoting compliance of patients to lipid-lowering therapy.
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Yu, Yan Nan, Ming-Li Li, Yu-Yuan Xu, Yao Meng, Harry Trieu, J. Pablo Villablanca, Shan Gao, Feng Feng, David S. Liebeskind, and Wei-Hai Xu. "Middle cerebral artery geometric features are associated with plaque distribution and stroke." Neurology 91, no. 19 (October 5, 2018): e1760-e1769. http://dx.doi.org/10.1212/wnl.0000000000006468.
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ObjectiveWe aimed to investigate the geometric features of the middle cerebral artery (MCA) and their relevance to plaque distribution and ischemic stroke.MethodsWe reviewed our institutional vessel wall imaging database. Patients with symptomatic MCA atherosclerosis, asymptomatic MCA atherosclerosis, or without MCA atherosclerosis were included. The MCA geometric features, including M1 segment shape and M1 curve orientation, were defined on magnetic resonance angiography. Plaque distribution and other plaque parameters were identified on vessel wall imaging. The association among MCA geometric features, plaque distribution, and ischemic stroke were analyzed.ResultsA total of 977 MCAs were analyzed (87 atherosclerotic symptomatic MCAs, 459 atherosclerotic asymptomatic MCAs, and 431 plaque-free MCAs). Overall, curved M1 segments were the predominant shape across all groups. In 91.1% of curved atherosclerotic MCAs, the plaque involved the inner wall of the curve. Plaque not involving the inner wall was shorter (p < 0.0001) and thinner (p = 0.005) compared to plaque involving the inner wall. Inferior plaque was observed in 39.9% of inferior-oriented M1 curves compared to 21.7% in non–inferior-oriented M1 curves (p < 0.0001). The absence of an inferior-oriented M1 curve (odds ratio 0.45, 95% confidence interval 0.27–0.77) and presence of superior plaque (odds ratio 2.67, 95% confidence interval 1.52–4.67) were independently associated with stroke after adjusting for plaque length and thickness, degree of stenosis, and remodeling ratio.ConclusionsMCA geometric features are associated with plaque distribution and stroke. Our findings provide insight into the vascular pathophysiology of MCA atherosclerosis.
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Li, Jiawen, Franco Centurion, Rouyan Chen, and Zi Gu. "Intravascular Imaging of Atherosclerosis by Using Engineered Nanoparticles." Biosensors 13, no. 3 (February 24, 2023): 319. http://dx.doi.org/10.3390/bios13030319.
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Atherosclerosis is a leading cause of morbidity and mortality, and high-risk atherosclerotic plaques can result in myocardial infarction, stroke, and/or sudden death. Various imaging and sensing techniques (e.g., ultrasound, optical coherence tomography, fluorescence, photoacoustic) have been developed for scanning inside blood vessels to provide accurate detection of high-risk atherosclerotic plaques. Nanoparticles have been utilized in intravascular imaging to enable targeted detection of high-risk plaques, to enhance image contrast, and in some applications to also provide therapeutic functions of atherosclerosis. In this paper, we review the recent progress on developing nanoparticles for intravascular imaging of atherosclerosis. We discuss the basic nanoparticle design principles, imaging modalities and instrumentations, and common targets for atherosclerosis. The review is concluded and highlighted with discussions on challenges and opportunities for bringing nanoparticles into in vivo (pre)clinical intravascular applications.
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Ait-Oufella, Hafid, Jean-Rémi Lavillegrand, and Alain Tedgui. "Regulatory T Cell-Enhancing Therapies to Treat Atherosclerosis." Cells 10, no. 4 (March 24, 2021): 723. http://dx.doi.org/10.3390/cells10040723.
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Experimental studies have provided strong evidence that chronic inflammation triggered by the sub-endothelial accumulation of cholesterol-rich lipoproteins in arteries is essential in the initiation and progression of atherosclerosis. Recent clinical trials highlighting the efficacy of anti-inflammatory therapies in coronary patients have confirmed that this is also true in humans Monocytes/macrophages are central cells in the atherosclerotic process, but adaptive immunity, through B and T lymphocytes, as well as dendritic cells, also modulates the progression of the disease. Analysis of the role of different T cell subpopulations in murine models of atherosclerosis identified effector Th1 cells as proatherogenic, whereas regulatory T cells (Tregs) have been shown to protect against atherosclerosis. For these reasons, better understanding of how Tregs influence the atherosclerotic process is believed to provide novel Treg-targeted therapies to combat atherosclerosis. This review article summarizes current knowledge about the role of Tregs in atherosclerosis and discusses ways to enhance their function as novel immunomodulatory therapeutic approaches against cardiovascular disease.
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Gasparyan, Armen Yuri. "The Use of Carotid Artery Ultrasonography in Different Clinical Conditions." Open Cardiovascular Medicine Journal 3, no. 1 (July 7, 2009): 78–80. http://dx.doi.org/10.2174/1874192400903010078.
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B-mode ultrasonography of the carotid artery is a non-invasive, informative and reproducible technique used for the assessment of prevalence and course of atherosclerosis in a variety of clinical conditions. Visualization of intima-media complex, atherosclerotic plaques, rough arterial wall and calcifications of the carotid artery may be useful for the assessment of atherosclerotic burden. The latter was confirmed in a recent consensus statement of the American Society of Echocardiography. Detection of structural changes, such as Menkeber’s sclerosis of the medial layer of the carotid artery, carotid aneurysm may indicate advanced vascular pathology and prompt an appropriate treatment. Ultrasound images of patients with atherosclerotic plaque and Menkeberg’s sclerosis are presented and issues related to clinical significance of the common carotid artery intima-media thickness are discussed.
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Jonik, Szymon, Michał Marchel, Marcin Grabowski, Grzegorz Opolski, and Tomasz Mazurek. "Gastrointestinal Incretins—Glucose-Dependent Insulinotropic Polypeptide (GIP) and Glucagon-like Peptide-1 (GLP-1) beyond Pleiotropic Physiological Effects Are Involved in Pathophysiology of Atherosclerosis and Coronary Artery Disease—State of the Art." Biology 11, no. 2 (February 11, 2022): 288. http://dx.doi.org/10.3390/biology11020288.
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Coronary artery disease (CAD), which is the manifestation of atherosclerosis in coronary arteries, is the most common single cause of death and is responsible for disabilities of millions of people worldwide. Despite numerous dedicated clinical studies and an enormous effort to develop diagnostic and therapeutic methods, coronary atherosclerosis remains one of the most serious medical problems of the modern world. Hence, new markers are still being sought to identify and manage CAD optimally. Trying to face this problem, we have raised the question of the most predominant gastrointestinal hormones; glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), mainly involved in carbohydrates disorders, could be also used as new markers of incidence, clinical course, and recurrence of CAD and are related to extent and severity of atherosclerosis and myocardial ischemia. We describe GIP and GLP-1 as expressed in many animal and human tissues, known to be connected to inflammation and related to enormous noncardiac and cardiovascular (CV) diseases. In animals, GIP and GLP-1 improve endothelial function and lead to reduced atherosclerotic plaque macrophage infiltration and stabilize atherosclerotic lesions by directly blocking monocyte migration. Moreover, in humans, GIPR activation induces the pro-atherosclerotic factors ET-1 (endothelin-1) and OPN (osteopontin) but also has anti-atherosclerotic effects through secretion of NO (nitric oxide). Furthermore, four large clinical trials showed a significant reduction in composite of CV death, MI, and stroke in long-term follow-up using GLP-1 analogs for DM 2 patients: liraglutide in LEADER, semaglutide in SUSTAIN-6, dulaglutide in REWIND and albiglutide in HARMONY. However, very little is known about GIP metabolism in the acute phase of myocardial ischemia or for stable patients with CAD, which constitutes a direction for future research. This review aims to comprehensively discuss the impact of GIP and GLP-1 on atherosclerosis and CAD and its potential therapeutic implications.
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Manea, Simona-Adriana, Mihaela-Loredana Vlad, Alexandra-Gela Lazar, Horia Muresian, Maya Simionescu, and Adrian Manea. "Pharmacological Inhibition of Lysine-Specific Demethylase 1A Reduces Atherosclerotic Lesion Formation in Apolipoprotein E-Deficient Mice by a Mechanism Involving Decreased Oxidative Stress and Inflammation; Potential Implications in Human Atherosclerosis." Antioxidants 11, no. 12 (December 1, 2022): 2382. http://dx.doi.org/10.3390/antiox11122382.
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Dysregulated epigenetic mechanisms promote transcriptomic and phenotypic alterations in cardiovascular diseases. The role of histone methylation-related pathways in atherosclerosis is largely unknown. We hypothesize that lysine-specific demethylase 1A (LSD1/KDM1A) regulates key molecular effectors and pathways linked to atherosclerotic plaque formation. Human non-atherosclerotic and atherosclerotic tissue specimens, ApoE-/- mice, and in vitro polarized macrophages (Mac) were examined. Male ApoE-/- mice fed a normal/atherogenic diet were randomized to receive GSK2879552, a highly specific LSD1 inhibitor, or its vehicle, for 4 weeks. The mRNA and protein expression levels of LSD1/KDM1A were significantly elevated in atherosclerotic human carotid arteries, atherosclerotic aortas of ApoE-/- mice, and M1-Mac. Treatment of ApoE-/- mice with GSK2879552 significantly reduced the extent of atherosclerotic lesions and the aortic expression of NADPH oxidase subunits (Nox1/2/4, p22phox) and 4-hydroxynonenal-protein adducts. Concomitantly, the markers of immune cell infiltration and vascular inflammation were significantly decreased. LSD1 blockade down-regulated the expression of genes associated with Mac pro-inflammatory phenotype. Nox subunit transcript levels were significantly elevated in HEK293 reporter cells overexpressing LSD1. In experimental atherosclerosis, LSD1 mediates the up-regulation of molecular effectors connected to oxidative stress and inflammation. Together, these data indicate that LSD1-pharmacological interventions are novel targets for supportive therapeutic strategies in atherosclerosis.
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Pitsilos, Stephanie, Jennifer Hunt, Emile Mohler, Anand Prabhakar, Mortimer Poncz, Jennine Dawicki, Tigran Khalapyan, et al. "Platelet factor 4 localization in carotid atherosclerotic plaques: correlation with clinical parameters." Thrombosis and Haemostasis 90, no. 12 (2003): 1112–20. http://dx.doi.org/10.1160/th03-02-0069.
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SummaryEmerging evidence supports a role for platelets in the progression of atherosclerosis in addition to an involvement in thrombotic vascular occlusion. Platelet Factor 4 (PF4), a chemokine released by activated platelets, stimulates several pro-atherogenic processes. Therefore, we examined the localization of PF4 and the homologous protein, Neutrophil Activating Protein-2 (NAP-2) in lesions representing the evolution of human atherosclerotic plaques. Carotid plaques from 132 patients with critical carotid stenosis and 6 autopsy specimens were studied. Clinical, histologic and immunohistochemical data were analyzed using a χ2-test. PF4 was detected in the cytoplasm of luminal and neovascular endothelium, in macrophages and in regions of plaque calcification. The presence of PF4 in macrophages and neovascular endothelium correlated with lesion grade (p = 0.004; p = 0.044). Staining of macrophages for PF4 correlated with the presence of symptomatic atherosclerotic disease (p = 0.028). In early lesions, PF4 was commonly found in macrophages of early lesions (Grade I/II), whereas NAP-2 was rarely present.In conclusion, correlation between PF4 deposition, lesion severity and symptomatic atherosclerosis suggests that persistent platelet activation may contribute to the evolution of athero-sclerotic vascular lesions. These studies support the rationale for the chronic use of anti-platelet therapy in patients at risk for developing symptomatic atherosclerosis.
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Sun, Changbin, Yahong Fu, Xia Gu, Xiangwen Xi, Xiang Peng, Chuhan Wang, Qi Sun, et al. "Macrophage-Enriched lncRNA RAPIA." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 6 (June 2020): 1464–78. http://dx.doi.org/10.1161/atvbaha.119.313749.
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Objective: Despite the current antiatherosclerotic and antithrombotic therapies, the incidence of advanced atherosclerosis-associated clinical events remains high. Whether long noncoding RNAs (lncRNAs) affect the progression of atherosclerosis and whether they are potential targets for the treatment of advanced atherosclerosis are poorly understood. Approach and Results: The progression of atherosclerotic lesions was accompanied by dynamic alterations in lncRNA expression, as revealed by RNA sequencing and quantitative polymerase chain reaction. Among the dynamically changing lncRNAs, we identified a novel lncRNA, lncRNA Associated with the Progression and Intervention of Atherosclerosis (RAPIA), that was highly expressed in advanced atherosclerotic lesions and in macrophages. Inhibition of RAPIA in vivo not only repressed the progression of atherosclerosis but also exerted atheroprotective effects similar to those of atorvastatin on advanced atherosclerotic plaques that had already formed. In vitro assays demonstrated that RAPIA promoted proliferation and reduced apoptosis of macrophages. A molecular sponge interaction between RAPIA and microRNA-183-5p was demonstrated by dual-luciferase reporter and RNA immunoprecipitation assays. Rescue assays indicated that RAPIA functioned at least in part by targeting the microRNA-183-5p/ITGB1 (integrin β1) pathway in macrophages. In addition, the transcription factor FoxO1 (forkhead box O1) could bind to the RAPIA promoter region and facilitate the expression of RAPIA. Conclusions: The progression of atherosclerotic lesions was accompanied by dynamic changes in the expression of lncRNAs. Inhibition of the pivotal lncRNA RAPIA may be a novel preventive and therapeutic strategy for advanced atherosclerosis, especially in patients resistant or intolerant to statins.
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Казакова, М. И., and Н. П. Митьковская. "Subclinical Coronary Atherosclerosis: Significance in Cardiovascular Risk Stratification." Кардиология в Беларуси, no. 4 (September 26, 2022): 482–91. http://dx.doi.org/10.34883/pi.2022.14.4.010.
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Сердечно-сосудистые заболевания остаются ведущей причиной заболеваемости и смертности во всем мире и в системе здравоохранения обуславливают самую высокую долю затрат. Патоморфологической основой ишемической болезни сердца в подавляющем большинстве клинических ситуаций является атеросклероз коронарных артерий. В последнее время множество исследований посвящено изучению ранней стадии атеросклероза – субклинического атеросклероза. Дестабилизация гемодинамически незначимых, бессимптомных атеросклеротических бляшек может привести к развитию инфаркта миокарда. В статье обсуждается распространенность, клиническая значимость необструктивного атеросклероза коронарных артерий. Отдельное внимание уделено шкалам стратификации сердечно-сосудистого риска. Обозначены современные методы диагностики коронарного атеросклероза, методы визуализации «нестабильных» атеросклеротических бляшек. В реальной клинической практике оценить «нестабильность» атеросклеротической бляшки не представляется возможным, поэтому сам факт наличия субклинического атеросклероза коронарных артерий позволяет отнести пациента к категории высокого и очень высокого риска. Cardiovascular diseases remain the leading cause of mortality and morbidity worldwide and represent the highest proportion of costs in healthcare systems. In the vast majority of cases, the pathomorphological basis of coronary heart disease is coronary artery atherosclerosis. Many of the recent research have been devoted to the study of the early stage of atherosclerosis – subclinical atherosclerosis. Destabilization of hemodynamically insignificant, asymptomatic atherosclerotic plaques can lead to the development of myocardial infarction. The article discusses the prevalence and clinical significance of non- obstructive atherosclerosis of the coronary arteries. Special attention is devoted to the scales of cardiovascular risk stratification. Modern methods of coronary atherosclerosis diagnosis, methods of visualization of unstable atherosclerotic plaques are outlined. Considering that it is impossible to assess the instability of atherosclerotic plaque in real clinical practice, the presence of subclinical coronary atherosclerosis itself allows the patient to be classified as high and very high risk.
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Singh, Laxman, Shikha Sharma, Suowen Xu, Devesh Tewari, and Jian Fang. "Curcumin as a Natural Remedy for Atherosclerosis: A Pharmacological Review." Molecules 26, no. 13 (July 1, 2021): 4036. http://dx.doi.org/10.3390/molecules26134036.
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Curcumin, a natural polyphenolic compound present in Curcuma longa L. rhizomes, shows potent antioxidant, anti-inflammatory, anti-cancer, and anti-atherosclerotic properties. Atherosclerosis is a comprehensive term for a series of degenerative and hyperplasic lesions such as thickening or sclerosis in large- and medium-sized arteries, causing decreased vascular-wall elasticity and lumen diameter. Atherosclerotic cerebro-cardiovascular disease has become a major concern for human health in recent years due to its clinical sequalae of strokes and heart attacks. Curcumin concoction treatment modulates several important signaling pathways related to cellular migration, proliferation, cholesterol homeostasis, inflammation, and gene transcription, among other relevant actions. Here, we provide an overview of curcumin in atherosclerosis prevention and disclose the underlying mechanisms of action of its anti-atherosclerotic effects.
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Bugger, Heiko, and Andreas Zirlik. "Anti-inflammatory Strategies in Atherosclerosis." Hämostaseologie 41, no. 06 (December 2021): 433–42. http://dx.doi.org/10.1055/a-1661-0020.
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AbstractAtherosclerotic vascular disease and its related complications are the major cause of mortality in Western societies. Atherosclerosis is a chronic inflammatory disease of the arterial wall triggered by traditional and nontraditional risk factors and mediated by inflammatory and immune responses. Recent clinical trials provided compelling evidence corroborating that atherosclerosis is an inflammatory disease and demonstrated efficacy of anti-inflammatory interventions in reducing cardiovascular events and mortality. Traditional risk factors drive vascular inflammation, further justifying the instrumental role of intensified risk factor management in attenuating and preventing atherosclerotic disease and complications. Promising therapeutic approaches specifically related to inhibition of inflammation span traditional anti-inflammatory drugs, specific immunomodulation, and development of vaccination against atherosclerotic disease. Here, we review the inflammatory component in atherogenesis, the available evidence from clinical trials evaluating efficacy of therapeutic anti-inflammatory interventions in patients with high cardiovascular risk, and discuss potential future targets for anti-inflammatory or immune modulatory treatment in atherosclerotic cardiovascular disease.
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Marcos-Jubilar, María, Josune Orbe, Carmen Roncal, Florencio J. D. Machado, José Antonio Rodriguez, Alejandro Fernández-Montero, Inmaculada Colina, Raquel Rodil, Juan C. Pastrana, and José A. Páramo. "Association of SDF1 and MMP12 with Atherosclerosis and Inflammation: Clinical and Experimental Study." Life 11, no. 5 (May 1, 2021): 414. http://dx.doi.org/10.3390/life11050414.
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BACKGROUND: Atherosclerosis is the main etiology of cardiovascular diseases (CVD), associated to systemic inflammation. Matrix metalloproteinases (MMPs) are related to atherosclerosis progression through the SDF1/CXCR4 axis promoting macrophages recruitment within the vascular wall. The goal was to assess new circulatory inflammatory markers in relation to atherosclerosis. METHODS: Measurement of SDF1, MMP12 and CRP in blood samples of 298 prospective patients with cardiovascular risk. To explore atherosclerosis progression, CXCR4/SDF1 axis and MMP12 expression were determined by RT-qPCR and by immunohistochemistry in the aorta of accelerated and delayed atherosclerosis mice models (Apoe-/- and Apoe-/-Mmp10-/-). RESULTS: SDF1, MMP12 and CRP were elevated in patients with clinical atherosclerosis, but after controlling by confounding factors, only SDF1 and CRP remained increased. Having high levels of both biomarkers showed 2.8-fold increased risk of presenting clinical atherosclerosis (p = 0.022). Patients with elevated SDF1, MMP12 and CRP showed increased risk of death in follow-up (HR = 3.2, 95%CI: 1.5–7.0, p = 0.004). Gene and protein expression of CXCR4 and MMP12 were increased in aortas from Apoe-/- mice. CONCLUSIONS: The combination of high circulating SDF1, MMP12 and CRP identified patients with particular inflammatory cardiovascular risk and increased mortality. SDF1/CXCR4 axis and MMP12 involvement in atherosclerosis development suggests that they could be possible atherosclerotic targets.
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Borcherding, Shawn M., Suzanne G. Meeves, Neil E. Klutman, and Patricia A. Howard. "Calcium-Channel Antagonists for Prevention of Atherosclerosis." Annals of Pharmacotherapy 27, no. 1 (January 1993): 61–67. http://dx.doi.org/10.1177/106002809302700115.
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OBJECTIVE: To critically evaluate the current literature regarding the role of calcium-channel antagonists in preventing atherosclerosis. DATA SOURCES: English language clinical studies, abstracts, conference proceedings, and review articles pertaining to calcium-channel antagonists and atherosclerosis. STUDY SELECTION: Relevant animal and human studies examining the role of calcium-channel antagonists in atherosclerosis prevention and treatment. DATA EXTRACTION: Potential mechanisms for the development of atherosclerosis and the use of calcium antagonists for preventing and treating coronary artery disease are discussed. Animal studies are summarized; next, significant data from human clinical studies are presented. DATA SYNTHESIS: Available studies are described and discussed. CONCLUSIONS: Results from animal and clinical trials in humans suggest that calcium antagonists may retard the development and progression of atherosclerosis. However, most clinical trials to date have been conducted in patients with proven atherosclerotic plaques. Further studies examining the role of calcium-channel antagonists in preventing and treating atherosclerosis are needed, but may be difficult to conduct because of the large numbers of patients required, long trial duration, and associated costs.
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Stakhneva, Ekaterina Mikhailovna, Evgeniia Vitalievna Striukova, and Yulia Igorevna Ragino. "Proteomic Studies of Blood and Vascular Wall in Atherosclerosis." International Journal of Molecular Sciences 22, no. 24 (December 9, 2021): 13267. http://dx.doi.org/10.3390/ijms222413267.
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The review is devoted to the analysis of literature data related to the role of proteomic studies in the study of atherosclerotic cardiovascular diseases. Diagnosis of patients with atherosclerotic plaques before clinical manifestations is an arduous task. The review presents the results of research on the new proteomic potential biomarkers of coronary heart disease, coronary atherosclerosis, acute coronary syndrome, myocardial infarction, carotid artery atherosclerosis. Also, the analysis of literature data on proteomic studies of the vascular wall was carried out. To assess the involvement of proteins in the pathological process of atherosclerosis, it is important to investigate the specific relationships between proteins in the arteries, expression and concentration of proteins. The development of proteomic technologies has made it possible to analyse the number of proteins associated with the development of the disease. Analysis of the proteomic profile of the vascular wall in atherosclerosis can help to detect possible diagnostically significant protein structures or potential biomarkers of the disease and develop novel approaches to the diagnosis of atherosclerosis and its complications.
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Watson, Shana R., and Susan M. Lessner. "(Second) Harmonic Disharmony: Nonlinear Microscopy Shines New Light on the Pathology of Atherosclerosis." Microscopy and Microanalysis 22, no. 3 (June 2016): 589–98. http://dx.doi.org/10.1017/s1431927616000842.
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AbstractThere has been increasing interest in second harmonic generation (SHG) imaging approaches for the investigation of atherosclerosis due to the deep penetration and three-dimensional sectioning capabilities of the nonlinear optical microscope. Atherosclerosis involves remodeling or alteration of the collagenous framework in affected vessels. The disease is often characterized by excessive collagen deposition and altered collagen organization. SHG has the capability to accurately characterize collagen structure, which is an essential component in understanding atherosclerotic lesion development and progression. As a structure-based imaging modality, SHG is most impactful in atherosclerosis evaluation in conjunction with other, chemically specific nonlinear optics (NLO) techniques to identify additional components of the lesion. These include the use of coherent anti-Stokes Raman scattering and two-photon excitation fluorescence for studying atherosclerosis burden, and application of stimulated Raman scattering to image cholesterol crystals. However, very few NLO studies have attempted to quantitate differences in control versus atherosclerotic states or to correlate the application to clinical situations. This review highlights the potential of SHG imaging to directly and indirectly describe atherosclerosis as a pathological condition.
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Binning, Mandy J., and Erol Veznedaroglu. "Endovascular Advances for Intracranial Occlusive Disease." Neurosurgery 74, suppl_1 (February 1, 2014): S126—S132. http://dx.doi.org/10.1227/neu.0000000000000149.
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Abstract Stroke is the fourth leading cause of death in the United States. Intracranial atherosclerotic disease accounts for 8%-10% of ischemic stroke in the United States. So far, surgical bypass has not proved to be superior to medical therapy. As both medical and endovascular therapies for intracranial atherosclerosis evolve, so too do the guidelines for treatment. Initial reports on the results of stent placement for symptomatic high-grade intracranial atherosclerotic disease were encouraging; however, recent trials suggest that initial medical management may be preferable. Currently, intracranial angioplasty and stenting for symptomatic intracranial atherosclerosis is now more controversial. Further trials are necessary to help determine which patients are ideal for endovascular therapies.
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Sharifullina, D. M., O. K. Pozdeev, R. M. Vasileva, and R. N. Khayrullin. "Blood microflora of patients with atherosclerotic vascular lesions and microflora of atherosclerotic plaques of carotid arteries." Ateroscleroz 17, no. 4 (January 12, 2022): 28–34. http://dx.doi.org/10.52727/2078-256x-2021-17-4-28-34.
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Aim of the study was to assess the frequency of microflora detection in the blood of patients with atherosclerotic vascular lesions and middle-aged patients without clinical symptoms of atherosclerosis. Compare the nature of microflora isolated from blood and the range of microorganisms isolated from atherosclerotic plaques (AP) of patients with carotid arteries atherosclerosis. Material and methods. The hemocultures of 118 men and 33 women with atherosclerosis (mean age 55.6 years) as well as 10 blood samples of 3 men and 7 women formed into a control group (mean age 37 years) were examined. Test samples were cultivated for 6 months. Tissue platings of carotid arteries AP in 11 women and 24 men of the main group (mean age 58.0) were incubated for 2 months. Methods based on Student’s t-test and Mann-Whitney U-test were used for statistical analysis of the obtained results. Results. Propionibacterium acnes hemocultures were detected in 9.9 % of patients from the main and control groups. In blood Staphylococcus epidermidis and Stenotrophomonas maltophylia were detected in 0.7 % of samples. P. acnes and Staphylococcus spp. cultures were obtained from AP in 34.3 and 45.7 %, including both microorganisms in 8.6 % of samples. Conclusions. P. acnes cultures are found equally frequently in the blood of atherosclerotic patients and patients not yet diagnosed with atherosclerosis. This study confirmed the presence of the same-name microorganisms in blood and atherosclerotic plaques. In 5.7 % (2 of 35) it was possible to extract simultaneously a P. acnes culture from two loci (atherosclerotic tissue and blood) in specific individuals. Further detailed research is required to study the etiological significance of the microbial factor in the atherosclerotic plaque formation.
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Alonso-Piñeiro, Jose Angel, Almudena Gonzalez-Rovira, Ismael Sánchez-Gomar, Juan Antonio Moreno, and Ma Carmen Durán-Ruiz. "Nrf2 and Heme Oxygenase-1 Involvement in Atherosclerosis Related Oxidative Stress." Antioxidants 10, no. 9 (September 14, 2021): 1463. http://dx.doi.org/10.3390/antiox10091463.
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Atherosclerosis remains the underlying process responsible for cardiovascular diseases and the high mortality rates associated. This chronic inflammatory disease progresses with the formation of occlusive atherosclerotic plaques over the inner walls of vascular vessels, with oxidative stress being an important element of this pathology. Oxidation of low-density lipoproteins (ox-LDL) induces endothelial dysfunction, foam cell activation, and inflammatory response, resulting in the formation of fatty streaks in the atherosclerotic wall. With this in mind, different approaches aim to reduce oxidative damage as a strategy to tackle the progression of atherosclerosis. Special attention has been paid in recent years to the transcription factor Nrf2 and its downstream-regulated protein heme oxygenase-1 (HO-1), both known to provide protection against atherosclerotic injury. In the current review, we summarize the involvement of oxidative stress in atherosclerosis, focusing on the role that these antioxidant molecules exert, as well as the potential therapeutic strategies applied to enhance their antioxidant and antiatherogenic properties.
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Kotova, Julia. "The Possible Role of Herpesviruses in the Pathogenesis of Coronary Atherosclerosis." International Journal of Biomedicine 11, no. 4 (December 10, 2021): 391–96. http://dx.doi.org/10.21103/article11(4)_ra1.
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Cardiovascular diseases are still the dominant cause of death worldwide. Coronary artery disease (CAD) is the most common type of heart disease and the leading cause of death for both men and women. Coronary atherosclerosis underlies multiple clinical manifestations ranging from asymptomatic to stable angina, acute coronary syndrome, MI, heart failure, and sudden cardiac death. The prerequisites for a closer study of the pathogenesis of the atherosclerotic process were the development of atherosclerotic vascular lesions at a younger age and the rapid progression of the process. Currently, it is generally accepted that CAD is a multifactorial disease. Attention is drawn to hereditary disorders of the receptor apparatus, endothelial dysfunction, and lipid metabolism disorders. In addition, latent viral infections are one of the etiopathogenetic factors in the development of atherosclerosis. A number of scientific studies have confirmed the relationship between infectious agents and the development of atherosclerotic vascular lesions. The viral etiology of the development and progression of atherosclerosis is the subject of debate among scientists around the world.
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Sui, Wenhai, Hongshi Li, Yunlong Yang, Xu Jing, Fei Xue, Jing Cheng, Mei Dong, et al. "Bladder drug mirabegron exacerbates atherosclerosis through activation of brown fat-mediated lipolysis." Proceedings of the National Academy of Sciences 116, no. 22 (May 13, 2019): 10937–42. http://dx.doi.org/10.1073/pnas.1901655116.
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Mirabegron (Myrbetriq) is a β3-adrenoreceptor agonist approved for treating overactive bladder syndrome in human patients. This drug can activate brown adipose tissue (BAT) in adult humans and rodents through the β3-adrenoreceptor-mediated sympathetic activation. However, the effect of the mirabegron, approved by the US Food and Drug Administration, on atherosclerosis-related cardiovascular disease is unknown. Here, we show that the clinical dose of mirabegron-induced BAT activation and browning of white adipose tissue (WAT) exacerbate atherosclerotic plaque development. In apolipoprotein E−/− (ApoE−/−) and low-density lipoprotein (LDL) receptor−/− (Ldlr−/−) mice, oral administration of clinically relevant doses of mirabegron markedly accelerates atherosclerotic plaque growth and instability by a mechanism of increasing plasma levels of both LDL-cholesterol and very LDL-cholesterol remnants. Stimulation of atherosclerotic plaque development by mirabegron is dependent on thermogenesis-triggered lipolysis. Genetic deletion of the critical thermogenesis-dependent protein, uncoupling protein 1, completely abrogates the mirabegron-induced atherosclerosis. Together, our findings suggest that mirabegron may trigger cardiovascular and cerebrovascular diseases in patients who suffer from atherosclerosis.
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Markina, Yuliya V., Tatiana V. Kirichenko, Alexander M. Markin, Irina Y. Yudina, Antonina V. Starodubova, Igor A. Sobenin, and Alexander N. Orekhov. "Atheroprotective Effects of Glycyrrhiza glabra L." Molecules 27, no. 15 (July 22, 2022): 4697. http://dx.doi.org/10.3390/molecules27154697.
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Cardiovascular diseases associated with atherosclerosis are the major cause of death in developed countries. Early prevention and treatment of atherosclerosis are considered to be an important aspect of the therapy of cardiovascular disease. Preparations based on natural products affect the main pathogenetic steps of atherogenesis, and so represent a perspective for the long-term prevention of atherosclerosis development. Numerous experimental and clinical studies have demonstrated the multiple beneficial effects of licorice and its bioactive compounds—anti-inflammatory, anti-cytokine, antioxidant, anti-atherogenic, and anti-platelet action—which allow us to consider licorice as a promising atheroprotective agent. In this review, we summarized the current knowledge on the licorice anti-atherosclerotic mechanisms of action based on the results of experimental studies, including the results of the in vitro study demonstrating licorice effect on the ability of blood serum to reduce intracellular cholesterol accumulation in cultured macrophages, and presented the results of clinical studies confirming the ameliorating activity of licorice in regard to traditional cardiovascular risk factors as well as the direct anti-atherosclerotic effect of licorice.
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Dinesch, Violeta, Mihail Dinesch, Ileana Voichita Sirbu, Cosmin Macarie, Bogdan Vasile Halatiu, and Mircea Buruian. "Predictors of Progression of Coronary Atherosclerosis after Percutaneous Coronary Intervention." Acta Medica Marisiensis 64, no. 3 (September 1, 2018): 103–7. http://dx.doi.org/10.2478/amma-2018-0020.
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AbstractObjective: This study investigated predictors of progression of coronary atherosclerosis after percutaneous coronary intervention. Their identification may be useful in clinical practice. Methods: We retrospectively reviewed the database of the Cardiology Department of the Cardiovascular Disease and Heart Transplant Institute in Tirgu Mures from January 2012 to December 2015 and identified 180 patients readmitted after successful percutaneous coronary intervention. The t-test, chi-square test, Fisher’s exact test, and mono- and multivariate analyses were used to evaluate associations between the patients’ clinical and angiographic characteristics and the progression of coronary atherosclerosis. Results: The pre-percutaneous coronary intervention atherosclerotic burden was associated with a higher number of new coronary lesions at readmission. Hypertension and the placement of more than one bare-metal stent in the right coronary artery were associated with increased odds of the progression of coronary atherosclerosis. The use of drug-eluting stents at the index percutaneous coronary intervention and a greater number of drug-eluting stents in the left anterior descending artery were associated with a decreased chance of the progression of coronary atherosclerosis. Conclusions: A massive atherosclerotic load at index percutaneous coronary intervention and hypertension were predictors of the progression of coronary artery atherosclerosis. The number, type, and localisation of the stent at the index percutaneous intervention could influence the progression of coronary atherosclerosis. Further research is needed to identify other potential predictors and to determine how to optimize the treatment of known predictors.
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Khabbaz Koche Ghazi, Mahdiyeh, Samad Ghaffari, Mohammad Naemi, Rezvaniyeh Salehi, Mohammadreza Taban Sadeghi, Meisam Barati, Alireza Namazi Shabestari, et al. "Effects of sodium selenite and selenium-enriched yeast on cardiometabolic indices of patients with atherosclerosis: A double-blind randomized clinical trial study." Journal of Cardiovascular and Thoracic Research 13, no. 4 (December 5, 2021): 314–19. http://dx.doi.org/10.34172/jcvtr.2021.51.
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Introduction: Atherosclerosis and related cardiovascular diseases (CVDs) are the major causes of mortality worldwide. The available reports regarding the effects of selenium (Se) supplementation in the realm of atherosclerosis have been equivocal. The present investigation is aimed to assess the effects of sodium selenite and Se-enriched yeast supplementation on metabolic parameters among atherosclerotic patients. Methods: In this double-blind placebo-controlled randomized clinical trial, 60 patients diagnosed with atherosclerosis were randomly allocated into either 200 μg/day selenite, yeast, or placebo groups for eight consecutive weeks. Serum levels of lipid profile and glycemic indices were measured at the baseline and end of the intervention. Results: There were no significant within-or between-group changes in levels of total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-c), fasting blood sugar, insulin, and homeostatic model assessment for IR throughout the study (P≥0.05). Only the low density lipoprotein cholesterol (LDL-c) levels were significantly lower in the yeast group in comparison with the placebo group (P= 0.015). Conclusion: The administration of Se-enriched yeast is significantly effective in decreasing LDL-c levels in patients with atherosclerosis. Additional clinical trial studies investigating the effect of Se administration on glucose homeostasis parameters and lipid profiles in atherosclerotic patients are suggested for a more definitive conclusion.
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Handa, R. "Cardiovascular co-morbidity in Asians with lupus: theoretical concern or clinical reality?" Lupus 19, no. 12 (October 2010): 1447–51. http://dx.doi.org/10.1177/0961203310374307.
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Immuno-inflammatory diseases like lupus are associated with premature atherosclerosis. With improved survival, atherosclerotic cardiovascular disease has emerged as an important late complication of systemic lupus erythematosus. The burden of this co-morbidity in Asian patients is not fully known but is likely to be high. We review the literature available and draw attention to this oft overlooked problem.