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m6A甲基化在心肌梗死后心肌重构发病机制中的研究进展OACSTPCD

Research progress in the role of m6A methylation in the pathogenesis of myocardial remodeling after myocardial infarction

中文摘要英文摘要

心肌梗死是心力衰竭最常见的病因,心肌梗死后可发生心肌重构,从而促进心力衰竭的进程.心肌梗死后心室重构的发生与m6A甲基化密切相关.m6A甲基化是一个可逆的高度动态变化的过程.该过程主要受m6A甲基化正负调控酶的介导,并通过细胞自噬等机制参与心肌梗死后心肌重构的发生.该文主要围绕近年来相关文献进行梳理,首先对m6A甲基化作以简介,然后对m6A甲基化酶调控心肌重构的作用进行介绍,最后从自噬、炎症、细胞凋亡、钙离子稳态、细胞外基质重塑和铁死亡等方面对m6A甲基化调控心肌重构的机制作总结性分析,并讨论了m6A甲基化血清学检测作为诊断心肌梗死后心肌重构的可行性,以期为相关研究提供参考.

Myocardial infarction is the most common cause of heart failure,and myocardial remodeling can occur after infarction,thus contributing to the progression of heart failure.The occurrence of post-infarction ventricular remode-ling is closely related to m6A methylation.m6A methylation is a reversible and highly dynamic process.This process is mainly mediated by m6A methylation positive and negative regulatory enzymes and is involved in the occurrence of post-in-farction myocardial remodeling through mechanisms such as cellular autophagy.This article mainly reviews relevant litera-ture in recent years.Firstly,a brief introduction is given to m6A methylation,followed by an introduction to the role of m6A methylase in regulating myocardial remodeling.Finally,a summary analysis is conducted on the mechanism of m6A methylation in regulating myocardial remodeling from the perspectives of autophagy,inflammation,cell apoptosis,calcium ion homeostasis,extracellular matrix remodeling,and ferroptosis.The feasibility of using m6A methylation serological de-tection as a diagnostic tool for myocardial remodeling after myocardial infarction is discussed,in order to provide reference for related research.

解长旭;郭帅杰;陈思琪;张蕾;刘卫红;李思耐;周明学

首都医科大学附属北京中医医院||北京市中医药研究所,北京市 100010

基础医学

m6A甲基化心肌梗死心肌重构心力衰竭

m6A methylationmyocardial infarctionmyocardial remodelingheart failure

《中国动脉硬化杂志》 2024 (007)

613-620 / 8

国家自然科学基金项目(82274287);北京市自然科学基金项目(7232266)

10.20039/j.cnki.1007-3949.2024.07.009

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