线粒体自噬在心肌缺血/再灌注损伤中的作用研究进展

doi:10.16352/j.issn.1001-6325.2023.11.1723

基础医学与临床 ›› 2023, Vol. 43 ›› Issue (11): 1723-1727.doi: 10.16352/j.issn.1001-6325.2023.11.1723

线粒体自噬在心肌缺血/再灌注损伤中的作用研究进展

马聪聪, 刘洋, 吕洋, 王海萍^*

河北北方学院干细胞与生殖生物学实验室,河北张家口 075000

收稿日期:2022-10-26 修回日期:2023-05-04 出版日期:2023-11-05 发布日期:2023-10-30
通讯作者: ^*haipingmimi@126.com
基金资助:
河北省自然科学基金(C2019405091);河北省高等学校科学技术研究项目(ZD2019066)

Progress on the role of mitophagy in myocardial ischemia-reperfusion injury

MA Congcong, LIU Yang, LYU Yang, WANG Haiping^*

Stem Cell and Reproductive Biology Laboratory, Hebei North University,Zhangjiakou,075000,China

Received:2022-10-26 Revised:2023-05-04 Online:2023-11-05 Published:2023-10-30
Contact: ^*haipingmimi@126.com

摘要/Abstract

摘要： 心肌缺血/再灌注损伤(MI/RI)时,可通过多种分子机制激活线粒体自噬。适度的线粒体自噬有助于维持线粒体膜电位,保护细胞膜结构和功能,从而减少MI/RI的发生。当线粒体功能出现紊乱,受损的线粒体不能充分清除或者线粒体自噬过度激活时,都会使MI/RI更严重。

关键词: 线粒体自噬, 心肌缺血/再灌注损伤(MI/RI), 分子机制, 信号通路

Abstract: Myocardial ischemia-reperfusion injury (MI/RI) is potentially associated with activation of mitophagy through a variety of molecular mechanisms. Moderate mitophagy is effective in maintaining mitochondrial membrane potential and cell membrane structure and function, thereby reducing MI/RI, whereas mitochondrial dysfunction, inadequate clearance or over-activated mitophagy can make MI/RI more severe.

Key words: mitophagy, myocardial ischemia-reperfusion injury (MI/RI), molecular mechanisms, signaling pathway

中图分类号:

马聪聪, 刘洋, 吕洋, 王海萍. 线粒体自噬在心肌缺血/再灌注损伤中的作用研究进展[J]. 基础医学与临床, 2023, 43(11): 1723-1727.

MA Congcong, LIU Yang, LYU Yang, WANG Haiping. Progress on the role of mitophagy in myocardial ischemia-reperfusion injury[J]. Basic & Clinical Medicine, 2023, 43(11): 1723-1727.

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线粒体自噬在心肌缺血/再灌注损伤中的作用研究进展

Progress on the role of mitophagy in myocardial ischemia-reperfusion injury

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