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Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury
Journal article   Open access   Peer reviewed

Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury

Kranti A. Mapuskar, Emily J. Steinbach, Amira Zaher, Dennis P. Riley, Robert A. Beardsley, Jeffery L. Keene, Jon T. Holmlund, Carryn M. Anderson, Diana Zepeda-Orozco, John M. Buatti, …
Antioxidants, Vol.10(9), p.1329
09/01/2021
DOI: 10.3390/antiox10091329
PMCID: PMC8469643
PMID: 34572961
url
https://doi.org/10.3390/antiox10091329View
Published (Version of record) Open Access

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.
Biochemistry & Molecular Biology Chemistry, Medicinal Food Science & Technology Life Sciences & Biomedicine Pharmacology & Pharmacy Science & Technology

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