Chinese Journal of Tissue Engineering Research ›› 2023, Vol. 27 ›› Issue (14): 2242-2248.doi: 10.12307/2023.180

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

Tan Xuefeng1, Ding Zhimin2, Guo Chenggen1, Sun Pu1   

  1. 1School of Physical Education and Sports, Beijing Normal University, Beijing 100875, China; 2School of Rehabilitation Medicine, Henan University of Chinese Medicine, Zhengzhou 450046, Henan Province, China
  • Received:2022-05-12 Accepted:2022-06-10 Online:2023-05-18 Published:2022-09-30
  • Contact: Sun Pu, Professor, Doctoral supervisor, School of Physical Education and Sports, Beijing Normal University, Beijing 100875, China
  • About author:Tan Xuefeng, Master candidate, School of Physical Education and Sports, Beijing Normal University, Beijing 100875, China
  • Supported by:
    Beijing Social Science Foundation in 2020, No. 20YTB012 (to SP)

Abstract: 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 ameliorates 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-reperfusion 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 exercises interfering with mitochondrial function after myocardial ischemia-reperfusion injury.
RESULTS AND CONCLUSION: With myocardial mitochondria as a target, exercise has been found to improve mitochondrial dysfunction after myocardial ischemia-reperfusion 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, thereby alleviating myocardial injury and promoting functional recovery.

Key words: myocardial ischemia-reperfusion injury, exercise, mitochondrial dysfunction, oxidative stress, apoptosis, quality control

CLC Number: