Wang Yonggang, Miao Xiao, Liu Yucheng, Li Fengsheng, Liu Quan, Sun Jian, Cai Lu
Cardiovascular Center, The First Hospital of Jilin University, 71 Xinmin Street, Changchun 130021, China ; Department of Pediatrics, Kosair Children Hospital Research Institute, University of Louisville, 570 South Preston Street, Baxter I, Suite 304F, Louisville, KY 40202, USA.
Department of Pediatrics, Kosair Children Hospital Research Institute, University of Louisville, 570 South Preston Street, Baxter I, Suite 304F, Louisville, KY 40202, USA ; The Second Hospital of Jilin University, Changchun 130041, China.
Oxid Med Cell Longev. 2014;2014:641979. doi: 10.1155/2014/641979. Epub 2014 Feb 18.
Cardiovascular disease (CVD) remains a leading cause of mortality worldwide despite advances in its prevention and management. A comprehensive understanding of factors which contribute to CVD is required in order to develop more effective treatment options. Dysregulation of epigenetic posttranscriptional modifications of histones in chromatin is thought to be associated with the pathology of many disease models, including CVD. Histone acetyltransferases (HATs) and deacetylases (HDACs) are regulators of histone lysine acetylation. Recent studies have implicated a fundamental role of reversible protein acetylation in the regulation of CVDs such as hypertension, pulmonary hypertension, diabetic cardiomyopathy, coronary artery disease, arrhythmia, and heart failure. This reversible acetylation is governed by enzymes that HATs add or HDACs remove acetyl groups respectively. New evidence has revealed that histone acetylation regulators blunt cardiovascular and related disease states in certain cellular processes including myocyte hypertrophy, apoptosis, fibrosis, oxidative stress, and inflammation. The accumulating evidence of the detrimental role of histone acetylation in cardiac disease combined with the cardioprotective role of histone acetylation regulators suggests that the use of histone acetylation regulators may serve as a novel approach to treating the millions of patients afflicted by cardiac diseases worldwide.
尽管在心血管疾病（CVD）的预防和管理方面取得了进展，但它仍然是全球主要的死亡原因。为了开发更有效的治疗方案，需要全面了解导致CVD的因素。染色质中组蛋白的表观遗传转录后修饰失调被认为与包括CVD在内的许多疾病模型的病理相关。组蛋白乙酰转移酶（HATs）和脱乙酰酶（HDACs）是组蛋白赖氨酸乙酰化的调节因子。最近的研究表明，可逆性蛋白质乙酰化在诸如高血压、肺动脉高压、糖尿病性心肌病、冠状动脉疾病、心律失常和心力衰竭等心血管疾病的调节中起重要作用。这种可逆性乙酰化分别由HATs添加或HDACs去除乙酰基的酶控制。新证据表明，组蛋白乙酰化调节剂在某些细胞过程（包括心肌细胞肥大、凋亡、纤维化、氧化应激和炎症）中可减轻心血管及相关疾病状态。组蛋白乙酰化在心脏病中的有害作用的证据不断积累，以及组蛋白乙酰化调节剂的心脏保护作用表明，使用组蛋白乙酰化调节剂可能是治疗全球数百万心脏病患者的一种新方法。
