Diabetic retinopathy is a complication of diabetes that damages the small blood vessels of the retina and can lead to vision loss and blindness. Research shows it progresses from an early non proliferative stage, where microaneurysms, hemorrhages, and lipid exudates appear, to more severe forms characterized by vascular closure, retinal ischemia, and eventually proliferative diabetic retinopathy with fragile new vessels that can bleed and cause retinal detachment.

Chronic hyperglycemia triggers oxidative stress, low grade inflammation, and biochemical changes such as activation of the polyol pathway, formation of advanced glycation end products, and protein kinase C signaling. These processes damage endothelial cells and pericytes, disrupt the blood retinal barrier, and alter retinal blood flow. Vascular endothelial growth factor plays a central role by driving abnormal neovascularization and vascular leakage.

Epidemiological studies confirm that both the duration of diabetes and the quality of glycemic control are key risk factors. Hypertension, hyperlipidemia, kidney disease, and pregnancy further increase risk and severity. Intensive control of blood glucose and blood pressure significantly reduces the incidence and progression of retinopathy.

Screening programs using fundus photography and optical coherence tomography enable early detection, which is crucial because symptoms often appear late. Treatment has shifted from destructive laser photocoagulation to targeted approaches. Intravitreal injections of anti VEGF agents are now first line therapy for diabetic macular edema and proliferative disease, often complemented by focal or panretinal laser and, in advanced cases, vitrectomy surgery. Ongoing research explores neuroprotective strategies, biomarkers for earlier prediction, and artificial intelligence systems to improve screening and personalized management.