AMPK/mTOR Signaling in Autophagy Regulation During Cisplatin-Induced Acute Kidney Injury

Ying Wang; Zhiwen Liu; Shaoqun Shu; Juan Cai; Chengyuan Tang; Zheng Dong

doi:10.3389/fphys.2020.619730

AMPK/mTOR Signaling in Autophagy Regulation During Cisplatin-Induced Acute Kidney Injury

Front Physiol. 2020 Dec 17:11:619730. doi: 10.3389/fphys.2020.619730. eCollection 2020.

Authors

Ying Wang¹, Zhiwen Liu¹, Shaoqun Shu¹, Juan Cai¹, Chengyuan Tang¹, Zheng Dong^{1

2}

Affiliations

¹ Department of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, China.
² Department of Cellular Biology and Anatomy, Charlie Norwood Veterans Affair Medical Center, Medical College of Georgia, Augusta University, Augusta, GA, United States.

Abstract

Autophagy is a conserved, multistep pathway that degrades and recycles dysfunctional organelles and macromolecules to maintain cellular homeostasis. Mammalian target of rapamycin (mTOR) and adenosine-monophosphate activated-protein kinase (AMPK) are major negative and positive regulators of autophagy, respectively. In cisplatin-induced acute kidney injury (AKI) or nephrotoxicity, autophagy is rapidly induced in renal tubular epithelial cells and acts as a cytoprotective mechanism for cell survival. Both mTOR and AMPK have been implicated in the regulation of autophagy in cisplatin-induced AKI. Targeting mTOR and/or AMPK may offer effective strategies for kidney protection during cisplatin-mediated chemotherapy.

Keywords: AMPK; acute kidney injury; autophagy; cisplatin; mTOR; nephrotoxicity.

Publication types

Review