《生命科学》 2023, 35(2): 173-184

运动调控衰老骨骼肌UPRmt和线粒体自噬互作的机制

王　艳^1,2 , 李佳林² , 王　哲² , 汪润姿² , 张子怡² , 薄　海^2,3,* , 张　勇^2,*

¹北京体育大学运动人体科学学院，北京 100084 ²天津体育学院运动健康学院，天津市运动生理学与运动医学重点实验室，天津 301617 ³武警后勤学院卫生勤务系，天津 300162

摘　要：

衰老性肌萎缩中的线粒体功能障碍与线粒体未折叠蛋白反应(mitochondrial unfolded protein response, UPRmt) 和线粒体自噬构成的线粒体质量控制(mitochondrial quality control, MQC) 的损伤密切相关。线粒体质量控制是线粒体维持内环境稳态的保护机制，其中UPRmt 和线粒体自噬分别负责受损线粒体的修复和清除。UPRmt 应对未折叠蛋白应激，维持线粒体和细胞蛋白质稳态，延长寿命并调节代谢重构，而线粒体自噬选择性地去除受损严重的线粒体，两者共同维护线粒体稳态。本文总结UPRmt 与线粒体自噬的互作、衰老骨骼肌UPRmt 与线粒体自噬的变化和运动逆转衰老骨骼肌UPRmt 和线粒体自噬的机制，重点总结运动源的活性氧(reactive oxygen species, ROS) 调控UPRmt 与线粒体自噬互作的信号通路研究进展，并为衰老性肌萎缩进程中线粒体质量控制的维持提供参考。

通讯作者：薄　海 , Email:bohaixd@126.com 张　勇 , Email:yzhang@tjus.edu.cn

The mechanisms of exercise-regulated interaction of UPRmt and mitophagy in aging skeletal muscle

WANG Yan^1,2 , LI Jia-Lin² , WANG Zhe² , WANG Run-Zi² , ZHANG Zi-Yi² , BO Hai^2,3,* , ZHANG Yong^2,*

¹School of Sport Science, Beijing Sport University, Beijing 100084, China ²Tianjin Key Laboratory of Exercise Physiology and Sports Medicine, School of Exercise & Health, Tianjin University of Sport, Tianjin 301617, China ³Department of Military Training Medicines, Logistics University of Chinese People’s Armed Police Force, Tianjin 300162, China

Abstract:

Mitochondrial dysfunction in sarcopenia is closely related to disruption of mitochondrial quality control (MQC) constituted by mitochondrial unfolded protein response (UPRmt) and mitophagy. MQC is a protective mechanism for mitochondria to maintain homeostasis. UPRmt and mitophagy are responsible for the repair and learance of mitochondrial damage, respectively. UPRmt responds to unfolded protein stress, maintains mitochondrial and cellular protein homeostasis, extends lifespan and regulates metabolic remodeling, while mitophagy selectively removes severely damaged mitochondria, both of which maintain mitochondrial homeostasis. This review summarizes the interaction between UPRmt and  mitophagy, the changes of UPRmt and mitophagy, and the regulation of exercise on reversing UPRmt and mitophagy in aging skeletal muscle, with a focus on the signaling pathway of exercise-derived reactive oxygen species (ROS) in an attempt to provide supportive evidence for the maintenance of mitochondrial quality control in the process of sarcopenia.

Communication Author：BO Hai , Email:bohaixd@126.com ZHANG Yong , Email:yzhang@tjus.edu.cn