PDF(Pubmed)
Abstract：
Histone deacetylases (HDAC) catalyze the removal of acetylation modifications on histones and non-histone proteins, which regulates gene expression and other cellular processes. HDAC inhibitors (HDACi), approved anti-cancer agents, emerge as a potential new therapy for heart diseases. Cardioprotective effects of HDACi are observed in many preclinical animal models of heart diseases. Genetic mouse models have been developed to understand the role of each HDAC in cardiac functions. Some of the findings are controversial. Here, we provide an overview of how HDACi and HDAC impact cardiac functions under physiological or pathological conditions. We focus on in vivo studies of zinc-dependent classical HDACs, emphasizing disease conditions involving cardiac hypertrophy, myocardial infarction (MI), ischemic reperfusion (I/R) injury, and heart failure. In particular, we review how non-biased omics studies can help our understanding of the mechanisms underlying the cardiac effects of HDACi and HDAC.
摘要：
组蛋白脱乙酰酶（HDAC）催化去除组蛋白和非组蛋白的乙酰化修饰，调节基因表达和其他细胞过程。HDAC抑制剂（HDACi），批准的抗癌剂，成为心脏病的潜在新疗法。在许多心脏疾病的临床前动物模型中观察到HDACi的心脏保护作用。已经开发了遗传小鼠模型来了解每种HDAC在心脏功能中的作用。一些发现是有争议的。这里,我们概述了HDACi和HDAC在生理或病理条件下如何影响心脏功能.我们专注于锌依赖性经典HDAC的体内研究，强调涉及心脏肥大的疾病，心肌梗死（MI），缺血再灌注（I/R）损伤，和心力衰竭。特别是,我们回顾了无偏组学研究如何帮助我们理解HDACi和HDAC心脏效应的潜在机制.
