Homo sapiens Variation. Homo sapiens

Dry eye disease (DED) is a common eye disease in clinical practice. Clinically available drugs are limited and their effects need to be improved. We provide complementary data for ferroptosis and autophagy in dry eye disease. More importantly, we revealed for the first time that AST efficiently protected corneal epithelial cells against ferroptosis in DED both in vitro and in vivo. AST extensively reduced excessive ROS production via SLC7A11/GPX4 pathway, rescued mitochondrial structure, restored defected autophagic flux in HCECs under hyperosmolarity. Thus, these data for the first time provide a novel therapy for DED treatment and elaborate greater understanding of pathogenesis.