Gene expression is needed for the maintenance of heart function under normal conditions and in response to stress. Each cell type of the heart has a specific program controlling transcription. Different types of stress induce modifications of these programs, and if prolonged, can lead to altered cardiac phenotype and, eventually, to heart failure. The transcriptional status of a gene is regulated by the epigenome, a complex network of DNA and histone modifications. Until a few years ago, our understanding of the role of the epigenome in heart disease was limited to that played by histone deacetylation. But over the last decade, the consequences for the maintenance of homeostasis in the heart and for the development of cardiac hypertrophy of a number of other modifications, including DNA methylation and hydroxymethylation, histone methylation and acetylation, and changes in chromatin architecture, have become better understood. Indeed, it is now clear that many levels of regulation contribute in defining the epigenetic landscape required for correct cardiomyocyte function, and that their perturbation is responsible for cardiac hypertrophy and fibrosis. Here, we review these aspects and draw a picture of what epigenetic modification may imply at the therapeutic level for heart failure.

中文翻译：

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表观基因组在心力衰竭中的作用。

在正常情况下和应对压力时，需要基因表达来维持心脏功能。心脏的每种细胞类型都有控制转录的特定程序。不同类型的压力会导致这些程序的改变，如果时间长，可能会导致心脏表型改变，最终导致心力衰竭。基因的转录状态由表观基因组，DNA和组蛋白修饰的复杂网络调节。直到几年前，我们对表观基因组在心脏病中的作用的了解还仅限于组蛋白脱乙酰作用。但是在过去的十年中，对心脏体内稳态的维持和心脏肥大的发展产生了许多其他影响，包括DNA甲基化和羟甲基化，组蛋白甲基化和乙酰化，以及染色质结构的变化，已被更好地理解。确实，现在很明显，许多水平的调节有助于定义正确的心肌细胞功能所需的表观遗传环境，并且它们的扰动是造成心脏肥大和纤维化的原因。在这里，我们回顾了这些方面，并画出了表观遗传修饰在心力衰竭的治疗水平上可能意味着什么。