Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury

Cisplatin is a chemotherapy agent commonly used to treat a wide variety of cancers. Despite the potential for both severe acute and chronic side effects, it remains a preferred therapeutic option for many malignancies due to its potent anti-tumor activity. Common cisplatin-associated side-effects in...
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Autor*in:	Kranti A. Mapuskar [verfasserIn] Emily J. Steinbach [verfasserIn] Amira Zaher [verfasserIn] Dennis P. Riley [verfasserIn] Robert A. Beardsley [verfasserIn] Jeffery L. Keene [verfasserIn] Jon T. Holmlund [verfasserIn] Carryn M. Anderson [verfasserIn] Diana Zepeda-Orozco [verfasserIn] John M. Buatti [verfasserIn] Douglas R. Spitz [verfasserIn] Bryan G. Allen [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	superoxide dismutase mitochondria reactive oxygen species mitochondrial metabolism superoxide cisplatin

Übergeordnetes Werk:	In: Antioxidants - MDPI AG, 2013, 10(2021), 9, p 1329
Übergeordnetes Werk:	volume:10 ; year:2021 ; number:9, p 1329

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/antiox10091329

Katalog-ID:	DOAJ049271873

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author	Kranti A. Mapuskar
spellingShingle	Kranti A. Mapuskar misc RM1-950 misc superoxide dismutase misc mitochondria misc reactive oxygen species misc mitochondrial metabolism misc superoxide misc cisplatin misc Therapeutics. Pharmacology Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury
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topic_title	RM1-950 Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury superoxide dismutase mitochondria reactive oxygen species mitochondrial metabolism superoxide cisplatin
topic	misc RM1-950 misc superoxide dismutase misc mitochondria misc reactive oxygen species misc mitochondrial metabolism misc superoxide misc cisplatin misc Therapeutics. Pharmacology
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title	Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury
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title_sort	mitochondrial superoxide dismutase in cisplatin-induced kidney injury
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title_auth	Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury
abstract	Cisplatin is a chemotherapy agent commonly used to treat a wide variety of cancers. Despite the potential for both severe acute and chronic side effects, it remains a preferred therapeutic option for many malignancies due to its potent anti-tumor activity. Common cisplatin-associated side-effects include acute kidney injury (AKI) and chronic kidney disease (CKD). These renal injuries may cause delays and potentially cessation of cisplatin therapy and have long-term effects on renal function reserve. Thus, developing mechanism-based interventional strategies that minimize cisplatin-associated kidney injury without reducing efficacy would be of great benefit. In addition to its action of cross-linking DNA, cisplatin has been shown to affect mitochondrial metabolism, resulting in mitochondrially derived reactive oxygen species (ROS). Increased ROS formation in renal proximal convoluted tubule cells is associated with cisplatin-induced AKI and CKD. We review the mechanisms by which cisplatin may induce AKI and CKD and discuss the potential of mitochondrial superoxide dismutase mimetics to prevent platinum-associated nephrotoxicity.
abstractGer	Cisplatin is a chemotherapy agent commonly used to treat a wide variety of cancers. Despite the potential for both severe acute and chronic side effects, it remains a preferred therapeutic option for many malignancies due to its potent anti-tumor activity. Common cisplatin-associated side-effects include acute kidney injury (AKI) and chronic kidney disease (CKD). These renal injuries may cause delays and potentially cessation of cisplatin therapy and have long-term effects on renal function reserve. Thus, developing mechanism-based interventional strategies that minimize cisplatin-associated kidney injury without reducing efficacy would be of great benefit. In addition to its action of cross-linking DNA, cisplatin has been shown to affect mitochondrial metabolism, resulting in mitochondrially derived reactive oxygen species (ROS). Increased ROS formation in renal proximal convoluted tubule cells is associated with cisplatin-induced AKI and CKD. We review the mechanisms by which cisplatin may induce AKI and CKD and discuss the potential of mitochondrial superoxide dismutase mimetics to prevent platinum-associated nephrotoxicity.
abstract_unstemmed	Cisplatin is a chemotherapy agent commonly used to treat a wide variety of cancers. Despite the potential for both severe acute and chronic side effects, it remains a preferred therapeutic option for many malignancies due to its potent anti-tumor activity. Common cisplatin-associated side-effects include acute kidney injury (AKI) and chronic kidney disease (CKD). These renal injuries may cause delays and potentially cessation of cisplatin therapy and have long-term effects on renal function reserve. Thus, developing mechanism-based interventional strategies that minimize cisplatin-associated kidney injury without reducing efficacy would be of great benefit. In addition to its action of cross-linking DNA, cisplatin has been shown to affect mitochondrial metabolism, resulting in mitochondrially derived reactive oxygen species (ROS). Increased ROS formation in renal proximal convoluted tubule cells is associated with cisplatin-induced AKI and CKD. We review the mechanisms by which cisplatin may induce AKI and CKD and discuss the potential of mitochondrial superoxide dismutase mimetics to prevent platinum-associated nephrotoxicity.
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title_short	Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury
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