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. 2021 Aug 5;9:706832. doi: 10.3389/fcell.2021.706832

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Copyright © 2021 Dai, Lu, Chen, Yang, Sun and He.

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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PINK1/Parkin-mediated mitophagy. The steps of mitophagy include the formation of the phagophore, autophagosome, autolysosome, and degradation of mitochondria. Damaged mitochondria that have lost their membrane potential (ψm) leads to PINK1 accumulation on the outer membrane surface. Then PINK1 recruits cytosolic Parkin, thereby phosphorylating. Activated Parkin contributes to the hyper-ubiquitination of OMM proteins, which are recognized by ubiquitin-binding adaptors, such as p62, NBR1, OPTN, and NDP52. These adaptor proteins induce the formation of autophagosomes by binging to LC3. The fusion of autophagosome and lysosome forms autolysosome in which enzymes are released to digest the contents and the nutrients and metabolites are recycled.