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. 2022 Feb 4;9:819454. doi: 10.3389/fcvm.2022.819454

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Copyright © 2022 Liu and Wu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mitophagy regulated by Fundc1 Pink/Parkin and BNIP3. Mitophagy is a biological process that selectively scavenges damaged mitochondria. It plays an important role in regulating the number of mitochondria in cells, maintaining the structure and function of mitochondria, and maintaining the homeostasis of cell energy metabolism. It is also an important mechanism for the quality control of mitochondria and plays an important role in the process of CHD accompanied by cardiomyocyte injury. Under CHD-induced stress, mitochondrial membrane potential decreases and ROS is overproduced, and the endoplasmic reticulum inputs more calcium ions into mitochondria. Driven by mitochondrial fission proteins drp1, MFF, and FIS1, mitochondria split into two sub mitochondria. Under the phosphorylation (dephosphorylation) of Fundc1 and the receptor regulation of BNIP3, the dysregulated daughter mitochondria react with LC3/LIR to form autophagic lysosomes. The ubiquitination of PINK/Parkin also mediates the formation of autophagic lysosomes. Under the regulation of mitophagy, damaged mitochondria are further cleared.