m6A甲基化在心力衰竭发病机制中的研究进展

Progress of m6A methylation in the pathogenesis of heart failure

摘要:

心力衰竭(HF)作为最严重的心血管疾病之一,近年来发病率持续上升。其发病机制与表观遗传学调控密切相关,其中N6-甲基腺苷(m⁶A)甲基化作为基因组中最常见的转录后表观遗传修饰,在HF的发生与发展过程中发挥重要作用。本文首先概述了m⁶A甲基转移酶、m⁶A去甲基化酶和m⁶A结合蛋白的基本概念,以及它们在HF发病机制中发挥的作用,然后从自噬、细胞凋亡、钙稳态和炎症反应等方面,探讨m⁶A甲基化在HF发病机制中的可能作用,以期为未来相关研究提供参考。

Abstract:

Heart failure (HF), as one of the most severe cardiovascular diseases, has shown a continuous rise in incidence in recent years. Its pathogenesis is closely associated with epigenetic regulation, among which N6-methyladenosine (m⁶A) methylation — the most common post-transcriptional epigenetic modification in the genome — plays a crucial role in the occurrence and progression of HF. This review first outlines the basic concepts of m⁶A methyltransferases, m⁶A demethylases, and m⁶A-binding proteins, as well as their roles in the pathogenesis of HF. Subsequently, it explores the potential mechanisms of m⁶A methylation in HF from aspects including autophagy, apoptosis, calcium homeostasis, and inflammatory response, aiming to provide a reference for future relevant research.