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首页> 外文期刊>Journal of Cellular Physiology >Epigenetics in Reactive and Reparative Cardiac Fibrogenesis: The Promise of Epigenetic Therapy
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Epigenetics in Reactive and Reparative Cardiac Fibrogenesis: The Promise of Epigenetic Therapy

机译：表观遗传学在反应和修复心脏纤维发生:表观遗传治疗的承诺

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摘要

Epigenetic changes play a pivotal role in the development of a wide spectrum of human diseases including cardiovascular diseases, cancer, diabetes, and intellectual disabilities. Cardiac fibrogenesis is a common pathophysiological process seen during chronic and stress-induced accelerated cardiac aging. While adequate production of extracellular matrix (ECM) proteins is necessary for post-injury wound healing, excessive synthesis and accumulation of extracellular matrix protein in the stressed or injured hearts causes decreased or loss of lusitropy that leads to cardiac failure. This self-perpetuating deposition of collagen and other matrix proteins eventually alter cellular homeostasis; impair tissue elasticity and leads to multi-organ failure, as seen during pathogenesis of cardiovascular diseases, chronic kidney diseases, cirrhosis, idiopathic pulmonary fibrosis, and scleroderma. In the last 25 years, multiple studies have investigated the molecular basis of organ fibrosis and highlighted its multi-factorial genetic, epigenetic, and environmental regulation. In this minireview, we focus on five major epigenetic regulators and discuss their central role in cardiac fibrogenesis. Additionally, we compare and contrast the epigenetic regulation of hypertension-induced reactive fibrogenesis and myocardial infarction-induced reparative or replacement cardiac fibrogenesis. As microRNAsone of the major epigenetic regulatorscirculate in plasma, we also advocate their potential diagnostic role in cardiac fibrosis. Lastly, we discuss the evolution of novel epigenetic-regulating drugs and predict their clinical role in the suppression of pathological cardiac remodeling, cardiac aging, and heart failure. J. Cell. Physiol. 232: 1941-1956, 2017. (c) 2016 Wiley Periodicals, Inc.
机译：表观遗传变化中发挥关键作用广泛的人类疾病的发展包括心血管疾病、癌症、糖尿病和智障。纤维发生是一种常见的病理生理看到在慢性应激过程心脏加速衰老。生产的细胞外基质(ECM)的蛋白质具有抑制受损伤口愈合,延伸是必要的过度的合成和积累紧张或细胞外基质蛋白受伤的心导致降低或丧失lusitropy导致心脏衰竭。自我的胶原蛋白和沉积其他矩阵最终改变细胞的蛋白质体内平衡;多器官衰竭,期间见过慢性心血管疾病的发病机制肾脏疾病、肝硬化、特发性肺纤维化和硬皮病。多个研究调查的分子器官纤维化和强调了它的基础现有的遗传、表观遗传和环境监管。关注五个主要监管机构和表观遗传讨论他们在心脏中心的作用纤维发生。对比的表观遗传调控降反应纤维发生和心肌infarction-induced修复或替代心脏纤维发生。主要的表观遗传regulatorscirculate等离子体,我们也提倡他们的潜力在心脏纤维化的诊断作用。讨论小说的演变epigenetic-regulating药物和预测他们的临床病理的抑制作用心脏重塑,心脏衰老,和心脏失败。(c) 2016年威利期刊公司。

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