NAT10 Promotes Tubular Epithelial Cell Senescence in Cisplatin-Induced Acute Kidney Injury by Regulating DDX17.

ABSTRACT: Acute kidney injury (AKI) is a severe clinical syndrome with high morbidity and mortality, yet its pathogenesis remains incompletely understood, and effective therapeutic strategies are still lacking. In this study, we observed significant upregulation of N-acetyltransferase 10 (NAT10) in the tubular epithelial cells of Cisplatin-induced AKI. Lentivirus-mediated knockdown of NAT10 or treatment with NAT10 inhibitor Remodelin, ameliorated Cisplatin-induced renal dysfunction and tubular injury. Importantly, NAT10 inhibition markedly attenuated cellular senescence in Cisplatin-induced AKI, as evidenced by reduced senescence-associated β-galactosidase (SA-β-gal) activity, downregulation of senescence markers (p53, p21 and γ-H2A.X) and decreased levels of senescence-associated secretory phenotyp

SUBMITTER: Zhu Y 

PROVIDER: S-EPMC12905645 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature