Prohibitin 2 ameliorates cisplatin-induced acute kidney injury by modulating mitochondrial homeostasis.

ABSTRACT: Acute kidney injury (AKI), associated with a major health burden globally, is frequently caused by nephrotoxic agents, specifically cisplatin. Prohibitin (PHB) 2, a highly conserved mitochondrial protein localized at the inner mitochondrial membrane, is key to maintaining mitochondrial respiration, cristae morphogenesis, and regulating cell death. Despite being extensively assessed in chronic kidney disease models, the role of PHB2 in AKI, particularly cisplatin-induced AKI, warrants further exploration. Here, we investigated the protective effects of PHB2 in cisplatin-induced AKI in in vitro and in vivo models. The results demonstrated that cisplatin upregulated PHB2 expression both in vitro and in vivo. Mechanistically, PHB2 deficiency exacerbated cisplatin-induced c

SUBMITTER: Zhang Q 

PROVIDER: S-EPMC12719072 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature