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. 2020 Aug 21;11:1992. doi: 10.3389/fmicb.2020.01992

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Copyright © 2020 Ren, Zhang, Ding, Zhong, Hu, Xu and Deng.

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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PTEN-induced protein kinase 1 (PINK1)/Parkin-mediated mitochondrial autophagy. (A) Under normal conditions, PINK1 is transferred to the inner mitochondrial membrane (IMM) by mitochondrial surface protein transporters, and it is degraded by presenilin-associated rhomboid like (PARL) protein. (B) Under stress conditions, PINK1 accumulates in the outer mitochondrial membrane (OMM) and recruits Parkin to phosphorylate it, after which Parkin ubiquitinates a variety of proteins on the mitochondrial surface. Autophagy then recognizes and encapsulates the ubiquitinated mitochondria.