Epigenetic modifications, such as histone or DNA modifications are key regulators of gene transcription and changes are often associated with maladaptive processes underlying cardiovascular disease. Epigenetic regulators therefore likely play a crucial role in cardiomyocyte homeostasis and facilitate the cellular adaption to various internal and external stimuli, responding to different intercellular and extracellular cues. Class IIa histone deacetylases are a class of epigenetic regulators that possess a myriad of post-transcriptional modification sites that modulate their activity in response to oxidative stress, altered catecholamine signalling or changes in the cellular metabolism. This review summaries the known reversible, post-translational modifications (PTMs) of class IIa histone deacetylases (HDACs) that ultimately drive transcriptional changes in homeostasis and disease. We also highlight the idea of a crosstalk of various PTMs on class IIa HDACs potentially leading to compensatory or synergistic effects on the class IIa HDAC-regulated cell behavior.

表观遗传修饰，例如组蛋白或 DNA 修饰是基因转录的关键调节因子，而变化通常与心血管疾病的适应不良过程有关。因此，表观遗传调节剂可能在心肌细胞稳态中发挥关键作用，促进细胞适应各种内部和外部刺激，响应不同的细胞间和细胞外信号。IIa 类组蛋白脱乙酰酶是一类表观遗传调节剂，具有大量转录后修饰位点，这些位点可调节其活性以响应氧化应激、改变的儿茶酚胺信号传导或细胞代谢的变化。这篇综述总结了已知的可逆性，IIa 类组蛋白去乙酰化酶 (HDAC) 的翻译后修饰 (PTM)，最终驱动体内平衡和疾病的转录变化。我们还强调了各种 PTM 对 IIa 类 HDAC 的串扰的想法，这可能导致对 IIa 类 HDAC 调节的细胞行为的补偿或协同效应。