| Literature DB >> 28024839 |
Chuanyan Zhao1, Zhuyun Chen1, Xueqiang Xu1, Xiaofei An2, Suyan Duan1, Zhimin Huang1, Chengning Zhang1, Lin Wu1, Bo Zhang1, Aihua Zhang3, Changying Xing4, Yanggang Yuan5.
Abstract
Cisplatin often causes acute kidney injury (AKI) in the treatment of a wide variety of malignancies. Mitochondrial dysfunction is one of the main reasons for cisplatin nephrotoxicity. Previous study showed that Pink1 and Parkin play central roles in regulating the mitophagy, which is a key protective mechanism by specifically eliminating dysfunctional or damaged mitochondria. However, the mechanisms that modulate mitophagy in cisplatin induced nephrotoxicity remain to be elucidated. The purpose of this study was to investigate the effects of Pink1/Parkin pathway in mitophagy, mitochondrial dysfunction and renal proximal tubular cells injury during cisplatin treatment. In cultured human renal proximal tubular cells, we found that knockdown of Pink1/Parkin induced the aggravation of mitochondrial function, leading to the increase of cell injury through inhibition of mitophagy. Additionally, the overexpression of Pink1/Parkin protected against cisplatin-induced mitochondrial dysfunction and cell injury by promoting mitophagy. Our results provide clear evidence that Pink1/Parkin-dependent mitophagy has identified potential targets for the treatment of cisplatin-induced AKI.Entities:
Keywords: AKI; Cisplatin; Mitochondrial dysfunction; Mitophagy; Parkin; Pink1
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Year: 2016 PMID： 28024839 DOI： 10.1016/j.yexcr.2016.12.015
Source DB: PubMed Journal: Exp Cell Res ISSN： 0014-4827 Impact factor: 3.905