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. 2019 Sep 25;10:1225. doi: 10.3389/fphys.2019.01225

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Copyright © 2019 Zhou, Zhang, Zhang, Yu, Sun, Zhu, Li, Liang, Han and Qin.

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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Schematic representation of possible mechanism related to mitophagy in cisplatin-induced kidney injury in PINK1 KO rats. Cisplatin causes the mitochondrial damage of renal tubular epithelial cells, which induces BNIP3/BNIP3L-mediated mitophagy, DRP1-mediated mitochondrial fission and apoptosis leading to kidney injury. And the excessive mitophagy may have negative feedback inhibition effect on the expression of PINK1 and Parkin and result in the down-regulation of PINK1 and Parkin in WT rats. In PINK1 KO rats, PINK1 deficiency causes a compensatory increase of Parkin and significantly inhibits the up-regulation of DRP1, which regulates mitochondrial fission and apoptosis, and therefore to inhibit the excessive mitophagy and overall kidney damage.