Astaxanthin activated the SLC7A11/GPX4 pathway to inhibit ferroptosis and enhance autophagy, ameliorating dry eye disease.

ABSTRACT: Dry eye disease (DED) is a common eye disease in clinical practice. The crucial pathogenesis of DED is that hyperosmolarity activates oxidative stress signaling pathways in corneal epithelial and immune cells and, thus, produces inflammatory molecules. The complex pathological changes in the dry eye still need to be elucidated to facilitate treatment. In this study, we found that astaxanthin (AST) can protect against DED through the SLC7A11/GPX4 pathway. After treatment with AST, the SLC7A11/GPX4 pathway was positively activated in DED both in vivo and in vitro, accompanied by enhanced autophagy and decreased ferroptosis. In hyperosmolarity-induced DED corneal epithelial cells, AST increased the expression of ferritin to promote iron storage and reduce Fe²⁺ overloa

SUBMITTER: Hou C 

PROVIDER: S-EPMC11366873 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature