运动调节线粒体功能改善心肌缺血再灌注损伤的研究进展  

Advances in exercise modulation of mitochondrial function to improve myocardial ischemia-reperfusion injury

作　　者：谭雪峰 丁志敏 郭成根 孙璞[1] Tan Xuefeng;Ding Zhimin;Guo Chenggen;Sun Pu(School of Physical Education and Sports,Beijing Normal University,Beijing 100875,China;School of Rehabilitation Medicine,Henan University of Chinese Medicine,Zhengzhou 450046,Henan Province,China)

机构地区：[1]北京师范大学体育与运动学院,北京市100875 [2]河南中医药大学康复医学院,河南省郑州市450046

出　　处：《中国组织工程研究》2023年第14期2242-2248,共7页Chinese Journal of Tissue Engineering Research

基　　金：2020年北京市社科基金规划项目(20YTB012),项目负责人:孙璞。

摘　　要：背景:心肌缺血再灌注损伤后线粒体功能障碍引发了线粒体氧化应激增加,诱发线粒体介导的细胞过度凋亡,导致线粒体质量控制失调,加重了心肌损伤程度。目的:阐述运动改善心肌缺血再灌注损伤导致的线粒体功能障碍的研究进展,为运动预防和缓解心肌缺血再灌注损伤提供理论依据。方法:检索Pub Med、Web of Science、CNKI、VIP和万方数据库收录的相关文献。以“运动、线粒体功能障碍、心肌缺血再灌注损伤”“氧化应激”“凋亡”“能量代谢”及“exercise,mitochondrial dysfunction,Myocardial ischemia-reperfusion injury,oxidative stress,apoptosis,energy metabolism”分别作为中、英文关键词进行文献检索,检索文献时限为2000年1月至2022年1月,系统总结不同运动类型干预心肌缺血再灌注损伤后线粒体功能的相关机制研究。结果与结论:以心肌线粒体为靶点,发现运动可改善心肌缺血再灌注损伤后线粒体功能障碍,其具体作用如下:运动可降低氧化应激水平,激活线粒体呼吸链促进心肌内线粒体生物发生,减少线粒体介导的细胞过度凋亡,促进线粒体动力学平衡,以及提高线粒体自噬活性控制心肌线粒体质量,以此缓解和帮助心肌损伤和恢复。BACKGROUND:Mitochondrial dysfunction after myocardial ischemia-reperfusion injury triggers an increase in mitochondrial oxidative stress,induces excessive mitochondria-mediated apoptosis,leads to dysregulation of mitochondrial quality control,and aggravates myocardial injury.OBJECTIVE:To clarify the research progress in exercise that amelio rates mitochondrial dysfunction caused by myocardial ischemia-reperfusion injury,providing a theoretical basis for exercise to prevent and alleviate myocardial ischemia-reperfusion injury.METHODS:PubMed,Web of science,CNKI,VIP,and WanFang databases were searched for relevant literature published from January 2000 to January 2022.Search terms included "exercise,mitochondrial dysfunction,myocardial ischemia-repe rfusion injury,oxidative stress,apoptosis,energy metabolism in Chinese and English,respectively.A systematical review was conducted and focused on the mechanism of different types of exe rcises interfering with mitochondrial function after myocardial ischemia-repe rfusion injury.RESULTS AND CONCLUSION:With myocardial mitochondria as a to rget,exercise has been found to improve mitochondrial dysfunction after myocardial ischemia-repe rfusion injury,with the following effects:exercise reduces oxidative stress levels,activates the mitochondrial respiratory chain to promote mitochondrial biogenesis in the myocardium,reduces mitochondria-mediated excessive apoptosis,promotes mitochondrial kinetic balance,and increases mitochondrial autophagic activity to control myocardial mitochondrial mass,there by alleviating myocardial injury and promoting functional recovery.

关 键 词：心肌缺血再灌注损伤 运动 线粒体功能障碍 氧化应激 细胞凋亡 质量控制 

分 类 号：R459.9[医药卫生—治疗学] R318[医药卫生—临床医学] R542.2