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Research progress in myocardial ischemia-reperfusion injury mediated by mitochondrial reactive oxygen species
Online published: 2021-06-29
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.
Ya-zhong WEI , Xiao-mei XUE , Bin HE . Research progress in myocardial ischemia-reperfusion injury mediated by mitochondrial reactive oxygen species[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2021 , 41(6) : 826 -829 . DOI: 10.3969/j.issn.1674-8115.2021.06.021
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