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Role of Mitophagy in Myocardial Ischemia/Reperfusion Injury and Chinese Medicine Treatment

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Abstract

Mitophagy is one of the important targets for the prevention and treatment of myocardial ischemia/reperfusion injury (MIRI). Moderate mitophagy can remove damaged mitochondria, inhibit excessive reactive oxygen species accumulation, and protect mitochondria from damage. However, excessive enhancement of mitophagy greatly reduces adenosine triphosphate production and energy supply for cell survival, and aggravates cell death. How dysfunctional mitochondria are selectively recognized and engulfed is related to the interaction of adaptors on the mitochondrial membrane, which mainly include phosphatase and tensin homolog deleted on chromosome ten (PTEN)-induced kinase 1/Parkin, hypoxia-inducible factor-1 α/Bcl-2 and adenovirus e1b19k Da interacting protein 3, FUN-14 domain containing protein 1 receptor-mediated mitophagy pathway and so on. In this review, the authors briefly summarize the main pathways currently studied on mitophagy and the relationship between mitophagy and MIRI, and incorporate and analyze research data on prevention and treatment of MIRI with Chinese medicine, thereby provide relevant theoretical basis and treatment ideas for clinical prevention of MIRI.

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Contributions

Xia JY drafted the manuscript. Li D and Lin Q helped the conception of design strategies. Chen C coordinated all manuscript and collected the data. Wan J, Li Y and Cui J revised the manuscript. All authors reviewed and approved the final manuscript.

Corresponding author

Correspondence to Dong Li.

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The authors declare that they have no competing interests.

Additional information

Supported by the Beijing University of Chinese Medicine Research and Innovation Team Project (No. 2019-JYB-TD-08) and Youth Science Fund Project of National Natural Science Foundation of China (No.81803906)

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Xia, Jy., Chen, C., Lin, Q. et al. Role of Mitophagy in Myocardial Ischemia/Reperfusion Injury and Chinese Medicine Treatment. Chin. J. Integr. Med. 29, 81–88 (2023). https://doi.org/10.1007/s11655-021-3301-1

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