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Mitophagy in Acute Kidney Injury and Kidney Repair

Acute kidney injury (AKI) is a major kidney disease characterized by rapid decline of renal function. Besides its acute consequence of high mortality, AKI has recently been recognized as an independent risk factor for chronic kidney disease (CKD). Maladaptive or incomplete repair of renal tubules af...

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Detalles Bibliográficos
Autores principales: Wang, Ying, Cai, Juan, Tang, Chengyuan, Dong, Zheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072358/
https://www.ncbi.nlm.nih.gov/pubmed/32024113
http://dx.doi.org/10.3390/cells9020338
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author Wang, Ying
Cai, Juan
Tang, Chengyuan
Dong, Zheng
author_facet Wang, Ying
Cai, Juan
Tang, Chengyuan
Dong, Zheng
author_sort Wang, Ying
collection PubMed
description Acute kidney injury (AKI) is a major kidney disease characterized by rapid decline of renal function. Besides its acute consequence of high mortality, AKI has recently been recognized as an independent risk factor for chronic kidney disease (CKD). Maladaptive or incomplete repair of renal tubules after severe or episodic AKI leads to renal fibrosis and, eventually, CKD. Recent studies highlight a key role of mitochondrial pathology in AKI development and abnormal kidney repair after AKI. As such, timely elimination of damaged mitochondria in renal tubular cells represents an important quality control mechanism for cell homeostasis and survival during kidney injury and repair. Mitophagy is a selective form of autophagy that selectively removes redundant or damaged mitochondria. Here, we summarize our recent understanding on the molecular mechanisms of mitophagy, discuss the role of mitophagy in AKI development and kidney repair after AKI, and present future research directions and therapeutic potential.
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spelling pubmed-70723582020-03-19 Mitophagy in Acute Kidney Injury and Kidney Repair Wang, Ying Cai, Juan Tang, Chengyuan Dong, Zheng Cells Review Acute kidney injury (AKI) is a major kidney disease characterized by rapid decline of renal function. Besides its acute consequence of high mortality, AKI has recently been recognized as an independent risk factor for chronic kidney disease (CKD). Maladaptive or incomplete repair of renal tubules after severe or episodic AKI leads to renal fibrosis and, eventually, CKD. Recent studies highlight a key role of mitochondrial pathology in AKI development and abnormal kidney repair after AKI. As such, timely elimination of damaged mitochondria in renal tubular cells represents an important quality control mechanism for cell homeostasis and survival during kidney injury and repair. Mitophagy is a selective form of autophagy that selectively removes redundant or damaged mitochondria. Here, we summarize our recent understanding on the molecular mechanisms of mitophagy, discuss the role of mitophagy in AKI development and kidney repair after AKI, and present future research directions and therapeutic potential. MDPI 2020-02-01 /pmc/articles/PMC7072358/ /pubmed/32024113 http://dx.doi.org/10.3390/cells9020338 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Wang, Ying
Cai, Juan
Tang, Chengyuan
Dong, Zheng
Mitophagy in Acute Kidney Injury and Kidney Repair
title Mitophagy in Acute Kidney Injury and Kidney Repair
title_full Mitophagy in Acute Kidney Injury and Kidney Repair
title_fullStr Mitophagy in Acute Kidney Injury and Kidney Repair
title_full_unstemmed Mitophagy in Acute Kidney Injury and Kidney Repair
title_short Mitophagy in Acute Kidney Injury and Kidney Repair
title_sort mitophagy in acute kidney injury and kidney repair
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072358/
https://www.ncbi.nlm.nih.gov/pubmed/32024113
http://dx.doi.org/10.3390/cells9020338
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