Bardoxolone methyl inhibits ferroptosis through the Keap1‑Nrf2 pathway in renal tubular epithelial cells.

ABSTRACT: Diabetic kidney disease (DKD), a primary cause of end‑stage kidney disease, involves ferroptosis in renal tubular epithelial cells (RTECs). Bardoxolone methyl (BM), known for its antioxidant and anti‑inflammatory properties, activates the Keap1‑Nrf2 pathway and has slows kidney function decline. 2‑Deoxy‑d‑ribose (dRib) can induce ferroptosis in RTECs by promoting the degradation of solute carrier family 7 member 11 (SLC7A11), a protein essential for cystine transport and glutathione (GSH) synthesis. The present study aimed to evaluate whether BM could inhibit dRib‑induced ferroptosis in RTECs and to elucidate the underlying mechanisms. Using NRK‑52E cells and primary RTECs, cystine uptake, GSH and iron levels, cell viability, lipid peroxidation and ferroptosis‑related markers were assessed

SUBMITTER: Yoo S 

PROVIDER: S-EPMC12319272 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature