线粒体自噬在肝脏缺血再灌注损伤中的作用

doi:10.16352/j.issn.1001-6325.2024.06.0877

基础医学与临床 ›› 2024, Vol. 44 ›› Issue (6): 877-881.doi: 10.16352/j.issn.1001-6325.2024.06.0877

线粒体自噬在肝脏缺血再灌注损伤中的作用

张祥鑫¹, 李文^2*

首都医科大学 1.2021级临床医学(5+3一体化);
2.基础医学院细胞生物学系,北京 100069

收稿日期:2023-11-29 修回日期:2024-01-24 出版日期:2024-06-05 发布日期:2024-05-24
通讯作者: ^*liwen@ccmu.edu.cn
基金资助:
国家自然科学基金(31771279)

Mitophagy in hepatic ischemia-reperfusion injury

ZHANG Xiangxin¹, LI Wen^2*

1. Department of Clinical Medicine (5+3 Integration),Grade 2021;
2. Department of Cell Biology, School of Basic Medical Science,Capital Medical University,Beijing 100069,China

Received:2023-11-29 Revised:2024-01-24 Online:2024-06-05 Published:2024-05-24
Contact: ^*liwen@ccmu.edu.cn

摘要/Abstract

摘要： 肝脏缺血再灌注损伤(HIRI)时,线粒体自噬可通过PINK1-Parkin、线粒体自噬受体等途径激活,并与线粒体动态平衡调节蛋白的表达密切相关。线粒体自噬是一把双刃剑,适度的线粒体自噬通过减轻氧化应激和维持线粒体稳态,起到减少肝细胞凋亡和坏死,抑制炎性反应,减轻HIRI的作用;而过度的线粒体自噬会加重HIRI。了解HIRI中线粒体自噬的调节机制和作用将为HIRI的防治提供新策略。

关键词: 肝脏缺血再灌注损伤, 线粒体自噬, 线粒体动态调节蛋白

Abstract: In case of hepatic ischemia-reperfusion injury (HIRI), mitophagy is induced by multiple pathways such as PINK1/Parkin and mitophagy receptor, which is closely related to mitochondrial dynamic related protein. Mitophagy is a double-edged sword. Moderate mitophagy is effective in reducing the oxidative stress and maintaining mitochondria homeostasis, thereby reducing hepatocyte apoptosis and necrosis, inhibiting inflammation response and mitigating HIRI. However excessive mitophagy will aggravate HIRI. So research on the role and mechanism of mitophagy may facilitate the development of new strategy for prevention and clinical treatment of HIRI.

Key words: hepatic ischemia-reperfusion injury (HIRI), mitophagy, mitochondrial dynamic related protein

中图分类号:

R364

张祥鑫, 李文. 线粒体自噬在肝脏缺血再灌注损伤中的作用[J]. 基础医学与临床, 2024, 44(6): 877-881.

ZHANG Xiangxin, LI Wen. Mitophagy in hepatic ischemia-reperfusion injury[J]. Basic & Clinical Medicine, 2024, 44(6): 877-881.

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线粒体自噬在肝脏缺血再灌注损伤中的作用

Mitophagy in hepatic ischemia-reperfusion injury

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