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Abstract
Retinopathies, including diabetic retinopathy, age-related macular degeneration, and retinopathy of prematurity, are leading causes of blindness in the U.S. and involve pathological neovascularization driven by VEGF. While VEGF regulation is classically attributed to Hypoxia Inducible Factor (HIF), we identify TEAD4 as a novel regulator. Using a murine oxygen-induced retinopathy model and Müller glia-like cell lines, we show TEAD4 activates VEGF promoters in both mouse and human, with enhanced activity under hypoxia via indirect modulation of HIF1α. TEAD4 expression in neovascular tufts suggests its role in retinal angiogenesis, highlighting TEAD4 as a potential therapeutic target for neovascular eye disease.