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Mitochondrial quality control in cardiac ischemia/reperfusion injury: new insights into mechanisms and implications

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Abstract

The current effective method for the treatment of myocardial infarction is timely restoration of the blood supply to the ischemic area of the heart. Although reperfusion is essential for reestablishing oxygen and nutrient supplies, it often leads to additional myocardial damage, creating an important clinical dilemma. Reports from long-term studies have confirmed that mitochondrial damage is the critical mechanism in cardiac ischemia/reperfusion (I/R) injury. Mitochondria are dynamic and possess a quality control system that targets mitochondrial quantity and quality by modifying mitochondrial fusion, fission, mitophagy, and biogenesis and protein homeostasis to maintain a healthy mitochondrial network. The system of mitochondrial quality control involves complex molecular machinery that is highly interconnected and associated with pathological changes such as oxidative stress, calcium overload, and endoplasmic reticulum (ER) stress. Because of the critical role of the mitochondrial quality control systems, many reports have suggested that defects in this system are among the molecular mechanisms underlying myocardial reperfusion injury. In this review, we briefly summarize the important role of the mitochondrial quality control in cardiomyocyte function and focus on the current understanding of the regulatory mechanisms and molecular pathways involved in mitochondrial quality control in cardiac I/R damage.

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Funding

This study was supported by grants from the National Natural Science Foundation of China (No. 81871592).

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Correspondence to Jun Ma.

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All the work reported in the manuscript is original and has not yet been submitted in other journal. Authors agree to transfer the copyright of manuscript to the Applied Biochemistry and Biotechnology Journal upon acceptance for publication.

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Headlights

1. Mitochondrial structure and function are regulated by mitochondrial fission and fusion.

2. New mitochondria are generated via mitochondrial biogenesis.

3. Upon mitochondrial stress, UPRmt is activated to restore mitochondrial proteomics.

4. Unrepairable mitochondria are removed via the process of mitophagy.

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Bai, Y., Wu, J., Yang, Z. et al. Mitochondrial quality control in cardiac ischemia/reperfusion injury: new insights into mechanisms and implications. Cell Biol Toxicol 39, 33–51 (2023). https://doi.org/10.1007/s10565-022-09716-2

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  • DOI: https://doi.org/10.1007/s10565-022-09716-2

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