JOURNAL OF SHANGHAI JIAOTONG UNIVERSITY (MEDICAL SCIENCE) ›› 2021, Vol. 41 ›› Issue (6): 826-829.doi: 10.3969/j.issn.1674-8115.2021.06.021

• Review • Previous Articles     Next Articles

Research progress in myocardial ischemia-reperfusion injury mediated by mitochondrial reactive oxygen species

Ya-zhong WEI(), Xiao-mei XUE, Bin HE()   

  1. Department of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200092, China
  • Online:2021-06-28 Published:2021-06-29
  • Contact: Bin HE;
  • Supported by:
    National Natural Science Foundation of China(82072199);Clinical Research Plan of Shanghai Hospital Development Center(SHDC2020CR3084B)


With the development of percutaneous coronary intervention technology, acute myocardial infarction has been effectively treated, but the myocardial ischemia-reperfusion injury (MIRI) has seriously affected the prognosis of patients. During the ischemia-reperfusion period of acute myocardial infarction, oxidative stress can seriously damage cardiac function. Excessive mitochondrial reactive oxygen species (mtROS) can affect mitochondrial permeability, and cause oxidative damage of specific molecules inside the mitochondria, which is the main driving factor for MIRI. In addition, mtROS can promote the signal transduction of inflammatory after myocardial infarction, regulate myocardial cell apoptosis, and participate in myocardial remodeling after myocardial infarction. This article reviews the mechanism of mtROS production in MIRI period and the clinical value and application prospect of reducing mtROS in the treatment of myocardial infarction.

Key words: myocardial ischemia-reperfusion injury (MIRI), mitochondria, reactive oxygen species (ROS)

CLC Number: