SIRT1 Prevents Ferroptosis in Corneal Epithelial Cells by Enhancing HIF1α Protein Stability in Dry Eye Disease - PubMed
4 hours ago
- #dry eye disease
- #SIRT1
- #ferroptosis
- Hyperosmotic stress from tear film instability worsens oxidative damage in corneal epithelial cells in dry eye disease (DED).
- Ferroptosis, an iron-dependent cell death mechanism driven by lipid peroxidation, plays a critical role in DED.
- SIRT1 downregulation under hyperosmotic stress promotes ferroptosis in corneal epithelial cells.
- SIRT1 positively regulates GPX4, a key mediator of ferroptosis, and its activation (e.g., via SRT1720) reduces oxidative damage and ferroptosis.
- SIRT1 stabilizes HIF1α by deacetylating it, preventing its degradation via the ubiquitin-proteasome pathway.
- The SIRT1-HIF1α axis enhances GPX4 levels, inhibiting ferroptosis and suggesting a therapeutic strategy for DED.