Function of histone methylation and acetylation modifiers in cardiac hypertrophy

Cardiac hypertrophy is an adaptive response of the heart to increased workload induced by various physiological or pathological stimuli. It is a common pathological process in multiple cardiovascular diseases, and it ultimately leads to heart failure. The development of cardiac hypertrophy is accompanied by gene expression reprogramming, a process that is largely dependent on epigenetic regulation. Histone modifications such as methylation and acetylation are dynamically regulated under cardiac stress. These consequently contribute to the pathogenesis of cardiac hypertrophy via compensatory or maladaptive transcriptome reprogramming. Histone methylation and acetylation modifiers play crucial roles in epigenetic remodeling during the pathogenesis of cardiac hypertrophy. Regulation of histone methylation and acetylation modifiers serves as a bridge between signal transduction and downstream gene reprogramming. Exploring the role of histone modifiers in cardiac hypertrophy provides novel therapeutic strategies to treat cardiac hypertrophy and heart failure. In this review, we summarize the recent advancements in functional histone methylation and acetylation modifiers in cardiac hypertrophy, with an emphasis on the underlying mechanisms and the therapeutic potential.

Automated summary

Cardiac hypertrophy is a common pathological process in cardiovascular diseases, characterized by gene expression reprogramming largely dependent on histone modifications such as methylation and acetylation. Understanding the role of histone modifiers in cardiac hypertrophy provides potential therapeutic strategies.