M6A甲基化在心衰中的研究进展  

Research Progress of M6A Methylation in Heart Failure

作　　者：王春艳 杨光[2] 付青青 

机构地区：[1]西安医学院研究生处,陕西 西安 [2]陕西省人民医院心血管内科,陕西 西安

出　　处：《临床医学进展》2024年第12期16-21,共6页Advances in Clinical Medicine

摘　　要：随着经济的发展,心力衰竭(HF)患者的死亡率仍持续增长。导致HF的病因众多,其中表观遗传和基因表达异常成为了HF的重要发病机制之一。N6-甲基腺苷(m6A)是真核细胞中最常见的内部RNA修饰,本篇综述将介绍m6A甲基转移酶(编码器writer),m6A去甲基化酶(消码器eraser),m6A识别蛋白(读码器 reader)通过一系列调节最终导致HF的发生。本篇综述还会介绍甲基化通过调节钙稳态、自噬及炎症反应、氧化应激以及铁死亡等介导HF的发生发展。With the development of the economy, the mortality rate of patients with heart failure (HF) remains high. There are many causes of HF, among which epigenetic and gene expression abnormalities have become one of the important pathogenesis of HF. N6-methyladenosine (m6A) is the most common internal RNA modification in eukaryotic cells, and this review will introduce m6A methyltransferase (encoder writer), m6A demethylase (decoder eraser), and m6A recognition protein (barcode reader) eventually lead to the development of HF by a series of modulations. This review will also cover that methylation may mediate the development of HF by modulating calcium homeostasis, autophagy and inflammatory responses, oxidative stress, and ferroptosis.

关 键 词：心力衰竭 M6A甲基化 钙稳态 自噬及炎症反应 氧化应激 铁死亡 

分 类 号：R73[医药卫生—肿瘤]