Additionally, TH, through the integrin αvβ3/PKD/HDAC5 pathway, upregulates bFGF to promote endothelial cell migration, proliferation, and angiogenesis, while high glucose and hypoxia induce VEGF and erythropoietin (EPO) expression, activating the integrin αvβ3/ERK1/2 pathway to drive pathological angiogenesis, and targeting integrin αvβ3 with Tetrac presents a potential therapeutic strategy for DR [151, 178, 179]; Oxidative stress: thyroid dysfunction can contribute to insulin resistance [180], dyslipidemia [181, 182], and oxidative stress [183, 184], collectively promoting vascular damage. This evidence concerns the gene EPO and metabolic syndrome.