Integrin β3 Promotes Retinal Neovascularization via Endoplasmic Reticulum Stress-Mediated Endothelial Cell Senescence - PubMed
5 hours ago
- #Retinal Neovascularization
- #Endothelial Senescence
- #Integrin β3
- Integrin β3 (ITGB3) is a transmembrane receptor involved in cell adhesion and signaling, which is implicated in retinal neovascularization (RNV).
- The study used an oxygen-induced retinopathy (OIR) mouse model to show that ITGB3 expression is significantly upregulated in endothelial cells (ECs), correlating with cellular senescence and endoplasmic reticulum stress (ERS).
- In vitro experiments with human retinal microvascular endothelial cells (HRMECs) demonstrated that ITGB3 knockdown suppresses migration, proliferation, and tube formation, key processes in angiogenesis.
- ITGB3 knockdown also reduced hypoxia-induced activation of the PERK/eIF2α/ATF4 ERS pathway and decreased markers of cellular senescence, including SA-β-Gal activity, p21, PAI-1, and SASP factors.
- The findings suggest that ITGB3 promotes RNV by inducing ERS-mediated endothelial cell senescence, highlighting the PERK/eIF2α/ATF4 pathway as a potential therapeutic target.