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

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 autophag...

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Autores principales: Wang, Ying, Liu, Zhiwen, Shu, Shaoqun, Cai, Juan, Tang, Chengyuan, Dong, Zheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7773913/
https://www.ncbi.nlm.nih.gov/pubmed/33391038
http://dx.doi.org/10.3389/fphys.2020.619730
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author Wang, Ying
Liu, Zhiwen
Shu, Shaoqun
Cai, Juan
Tang, Chengyuan
Dong, Zheng
author_facet Wang, Ying
Liu, Zhiwen
Shu, Shaoqun
Cai, Juan
Tang, Chengyuan
Dong, Zheng
author_sort Wang, Ying
collection PubMed
description 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.
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spelling pubmed-77739132021-01-01 AMPK/mTOR Signaling in Autophagy Regulation During Cisplatin-Induced Acute Kidney Injury Wang, Ying Liu, Zhiwen Shu, Shaoqun Cai, Juan Tang, Chengyuan Dong, Zheng Front Physiol Physiology 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. Frontiers Media S.A. 2020-12-17 /pmc/articles/PMC7773913/ /pubmed/33391038 http://dx.doi.org/10.3389/fphys.2020.619730 Text en Copyright © 2020 Wang, Liu, Shu, Cai, Tang and Dong. http://creativecommons.org/licenses/by/4.0/ 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.
spellingShingle Physiology
Wang, Ying
Liu, Zhiwen
Shu, Shaoqun
Cai, Juan
Tang, Chengyuan
Dong, Zheng
AMPK/mTOR Signaling in Autophagy Regulation During Cisplatin-Induced Acute Kidney Injury
title AMPK/mTOR Signaling in Autophagy Regulation During Cisplatin-Induced Acute Kidney Injury
title_full AMPK/mTOR Signaling in Autophagy Regulation During Cisplatin-Induced Acute Kidney Injury
title_fullStr AMPK/mTOR Signaling in Autophagy Regulation During Cisplatin-Induced Acute Kidney Injury
title_full_unstemmed AMPK/mTOR Signaling in Autophagy Regulation During Cisplatin-Induced Acute Kidney Injury
title_short AMPK/mTOR Signaling in Autophagy Regulation During Cisplatin-Induced Acute Kidney Injury
title_sort ampk/mtor signaling in autophagy regulation during cisplatin-induced acute kidney injury
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7773913/
https://www.ncbi.nlm.nih.gov/pubmed/33391038
http://dx.doi.org/10.3389/fphys.2020.619730
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