Angiotensin II-Induced Ferroptosis in Epithelial Cells Contributes to Kidney Injury via SP1-DPEP1-Mediated SLC3A2 Degradation.

ABSTRACT: Angiotensin II (AngII) activation, a key driver of diabetes pathogenesis and associated complications, induces kidney injury by promoting oxidative stress and inflammation. Ferroptosis is an iron-dependent regulated cell death, playing a crucial role in kidney injury. This study aimed to explore the contribution of ferroptosis to AngII-induced kidney injury and its regulatory mechanisms. Our findings reveal that chronic AngII stimulation leads to renal dysfunction, characterized by elevated serum creatinine levels, increased urinary protein-to-creatinine ratio, and tubular injury. These changes are associated with ferroptosis in renal tubular epithelial cells (TECs) and a marked upregulation of dipeptidase 1 (DPEP1) expression. Notably, the ferroptosis inhibitor ferrostatin-1 (Fer-1) effec

SUBMITTER: Tian Y 

PROVIDER: S-EPMC12928747 | biostudies-literature | 2026 Mar

REPOSITORIES: biostudies-literature