AKR1C1 Protects Corneal Epithelial Cells Against Oxidative Stress-Mediated Ferroptosis in Dry Eye

Abstract

Excessive oxidative stress-induced ferroptosis participates in DED pathogenesis. The expression of AKR1C1 is triggered by NRF2 to decrease ferroptosis-induced cell damage and inflammation in HCECs. These findings may provide potential makers targeting ferroptosis and AKR1C1 for DED therapy.