Roles of Reactive Oxygen Species and Autophagy in the Pathogenesis of Cisplatin-Induced Acute Kidney Injury

Cisplatin-induced acute kidney injury (AKI) is the main factor restraining the clinical application of cisplatin. The AKI is associated with high mortality and morbidity, but no effective pharmacological treatment is available at present. As increased levels of reactive oxygen species (ROS) may prom...

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Main Authors: Sayuri Yoshikawa, Kurumi Taniguchi, Haruka Sawamura, Yuka Ikeda, Ai Tsuji, Satoru Matsuda
Format: Article
Language:English
Published: MDPI AG 2022-08-01
Series:Oxygen
Subjects:
Online Access:https://www.mdpi.com/2673-9801/2/3/22
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author Sayuri Yoshikawa
Kurumi Taniguchi
Haruka Sawamura
Yuka Ikeda
Ai Tsuji
Satoru Matsuda
author_facet Sayuri Yoshikawa
Kurumi Taniguchi
Haruka Sawamura
Yuka Ikeda
Ai Tsuji
Satoru Matsuda
author_sort Sayuri Yoshikawa
collection DOAJ
description Cisplatin-induced acute kidney injury (AKI) is the main factor restraining the clinical application of cisplatin. The AKI is associated with high mortality and morbidity, but no effective pharmacological treatment is available at present. As increased levels of reactive oxygen species (ROS) may promote the progression of the injury, the elimination of ROS has been considered as an effective method to prevent the cisplatin-induced AKI. In addition, it has been revealed that an inducer of autophagy could protect kidney cells in the autophagy dependent manner. Induction of autophagy could also modulate the production of ROS in cases of renal injury. Therefore, kidney-targeted antioxidants and/or autophagy are urgently required for the better treatment of AKI. Accumulating evidence has indicated the important roles of gut microbiota in the pathogenesis of AKI. In addition, there is a scientific basis for considering future clinical applications of probiotics and/or prebiotics to treat cisplatin-induced AKI. Thus, gut microbiota might be a promising therapeutic target via the alteration of autophagy for the cancer therapy-induced nephrotoxicity.
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spelling doaj.art-74d21eaa3dd949c2828edf1373e443ff2023-11-24T09:33:45ZengMDPI AGOxygen2673-98012022-08-012331732610.3390/oxygen2030022Roles of Reactive Oxygen Species and Autophagy in the Pathogenesis of Cisplatin-Induced Acute Kidney InjurySayuri Yoshikawa0Kurumi Taniguchi1Haruka Sawamura2Yuka Ikeda3Ai Tsuji4Satoru Matsuda5Department of Food Science and Nutrition, Nara Women’s University, Kita-Uoya Nishimachi, Nara 630-8506, JapanDepartment of Food Science and Nutrition, Nara Women’s University, Kita-Uoya Nishimachi, Nara 630-8506, JapanDepartment of Food Science and Nutrition, Nara Women’s University, Kita-Uoya Nishimachi, Nara 630-8506, JapanDepartment of Food Science and Nutrition, Nara Women’s University, Kita-Uoya Nishimachi, Nara 630-8506, JapanDepartment of Food Science and Nutrition, Nara Women’s University, Kita-Uoya Nishimachi, Nara 630-8506, JapanDepartment of Food Science and Nutrition, Nara Women’s University, Kita-Uoya Nishimachi, Nara 630-8506, JapanCisplatin-induced acute kidney injury (AKI) is the main factor restraining the clinical application of cisplatin. The AKI is associated with high mortality and morbidity, but no effective pharmacological treatment is available at present. As increased levels of reactive oxygen species (ROS) may promote the progression of the injury, the elimination of ROS has been considered as an effective method to prevent the cisplatin-induced AKI. In addition, it has been revealed that an inducer of autophagy could protect kidney cells in the autophagy dependent manner. Induction of autophagy could also modulate the production of ROS in cases of renal injury. Therefore, kidney-targeted antioxidants and/or autophagy are urgently required for the better treatment of AKI. Accumulating evidence has indicated the important roles of gut microbiota in the pathogenesis of AKI. In addition, there is a scientific basis for considering future clinical applications of probiotics and/or prebiotics to treat cisplatin-induced AKI. Thus, gut microbiota might be a promising therapeutic target via the alteration of autophagy for the cancer therapy-induced nephrotoxicity.https://www.mdpi.com/2673-9801/2/3/22cisplatinreactive oxygen speciesautophagyhistone deacetylasescanceracute kidney injury
spellingShingle Sayuri Yoshikawa
Kurumi Taniguchi
Haruka Sawamura
Yuka Ikeda
Ai Tsuji
Satoru Matsuda
Roles of Reactive Oxygen Species and Autophagy in the Pathogenesis of Cisplatin-Induced Acute Kidney Injury
Oxygen
cisplatin
reactive oxygen species
autophagy
histone deacetylases
cancer
acute kidney injury
title Roles of Reactive Oxygen Species and Autophagy in the Pathogenesis of Cisplatin-Induced Acute Kidney Injury
title_full Roles of Reactive Oxygen Species and Autophagy in the Pathogenesis of Cisplatin-Induced Acute Kidney Injury
title_fullStr Roles of Reactive Oxygen Species and Autophagy in the Pathogenesis of Cisplatin-Induced Acute Kidney Injury
title_full_unstemmed Roles of Reactive Oxygen Species and Autophagy in the Pathogenesis of Cisplatin-Induced Acute Kidney Injury
title_short Roles of Reactive Oxygen Species and Autophagy in the Pathogenesis of Cisplatin-Induced Acute Kidney Injury
title_sort roles of reactive oxygen species and autophagy in the pathogenesis of cisplatin induced acute kidney injury
topic cisplatin
reactive oxygen species
autophagy
histone deacetylases
cancer
acute kidney injury
url https://www.mdpi.com/2673-9801/2/3/22
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