摘要
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.
作者
彭泽琳
李旻俊
张良清
PENG Zelin;LI Minjun;ZHANG Liangqing(Department of Anesthesiology,Affiliated Hospital of Guangdong Medical University,Zhanjiang 524000,China)
出处
《中华实用诊断与治疗杂志》
2020年第11期1185-1188,共4页
Journal of Chinese Practical Diagnosis and Therapy
基金
国家自然科学基金(81470405)。
关键词
心肌缺血再灌注损伤
自噬
N6-甲基腺苷
myocardial ischemia-reperfusion injury
autophagy
N6-methyladenosine