Volume 20 Issue 7
Jul.  2022
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ZHANG Wen-jing, LI Xiao-feng, SUN Ming-ming, PENG Hu. Research progress and function of mitophagy in myocardial infarction[J]. Chinese Journal of General Practice, 2022, 20(7): 1194-1198. doi: 10.16766/j.cnki.issn.1674-4152.002556
Citation: ZHANG Wen-jing, LI Xiao-feng, SUN Ming-ming, PENG Hu. Research progress and function of mitophagy in myocardial infarction[J]. Chinese Journal of General Practice, 2022, 20(7): 1194-1198. doi: 10.16766/j.cnki.issn.1674-4152.002556

Research progress and function of mitophagy in myocardial infarction

doi: 10.16766/j.cnki.issn.1674-4152.002556
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  • Received Date: 2022-02-08
    Available Online: 2022-09-23
  • Myocardial infarction (MI) refers to myocardial ischemic necrosis caused by persistent and severe acute ischemia and hypoxia caused by acute reduction or interruption of perfusion blood flow after the coronary artery that nourishes the heart. The mechanism of myocardial injury in patients with MI needs to be clarified urgently. The research on the mechanism of MI and the search for intervention targets have important clinical value. The mitochondria, as organelles that provide energy, is the key organelles for the continuous contraction and relaxation of cardiac muscle cells. They are responsible for adenosine triphosphate generation and energy metabolism. The loss of mitochondrial integrity and function is a key pathological factor that changes the structure and function of the heart. Mitochondrial dysfunction during MI is an important mechanism of myocardial injury. Mitochondrial quality control refers to maintaining a balance between mitochondrial production and clearance, which is particularly essential for maintaining cell survival and function. Mitophagy is associated with various diseases, such as neurodegenerative diseases, cardiovascular diseases and cancer. Mitophagy is a selective autophagy that uses damaged mitochondria as an autophagy substrate to maintain cardiovascular homeostasis. Mitophagy controls the quality of the mitochondria by promoting the degradation and recycling of damaged mitochondria and protects cardiomyocytes from ischemic injury. For normal cardiomyocytes, sufficient mitochondrial production could ensure sufficient energy supply. However, in the process of MI, mitochondrial damage occurs in cardiomyocytes and if the damaged mitochondria are not cleared in time, cardiomyocyte damage and even apoptosis could be induced. The process of mitophagy is complex, involving many physiological and pathological processes, and it is regulated by various substances, such as proteins and RNAs. In this article, the important roles and related mechanisms of mitophagy in MI are reviewed.

     

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