N6-甲基腺苷调控细胞自噬在心肌缺血再灌注损伤机制中作用的研究进展

Role of N6-methyladenosine in regulating autophagy in myocardial ischemia-reperfusion injury

心肌缺血再灌注损伤是缺血性心脏病治疗中的难点,其发生机制中自噬起重要作用。自噬是真核细胞存在的一种防御和应激调控机制,通过溶酶体途径降解受损蛋白质和细胞器等进行“自我消化”。N6-甲基腺苷修饰是真核生物信使RNA常见的一种转录后修饰,在自噬调控中的作用和分子机制较复杂。本文就N6-甲基腺苷调控细胞自噬、参与心肌缺血再灌注损伤的潜在机制的研究进展作一综述。

Myocardial ischemia-reperfusion injury is a difficult point in the treatment of ischemic heart disease,and autophagy plays an important role in its mechanism.Autophagy is a defense and stress regulation mechanism in eukaryotic cells and degrades damaged proteins and organelles through the lysosomal pathway for“self-digestion”.N6-methyladenosine modification is a common post-transcriptional modification of eukaryotic messenger RNA,and it has complicated role and molecular mechanism in the regulation of autophagy.This paper reviews the research progress of the potential mechanism of N6-methyladenosine in regulating cell autophagy and participating in myocardial ischemiareperfusion injury.