Background: Diabetic retinopathy (DR) is a microvascular and neurodegenerative complication of diabetes and remains a leading cause of preventable visual impairment in working-age adults. Because the number of people living with diabetes continues to grow, the absolute burden of DR is expected to rise for decades.
Objective: This review summarises the molecular and cellular mechanisms that drive DR, maps them onto established and emerging pharmacological targets, and appraises the clinical evidence for current drug-based management.
Findings: Chronic hyperglycaemia activates several interconnected injury pathways (polyol flux, advanced glycation, protein kinase C activation, oxidative stress and low-grade inflammation) that converge on endothelial dysfunction, pericyte loss, breakdown of the blood–retinal barrier and, in advanced disease, VEGF-driven neovascularisation. Systemic control of glucose, blood pressure and lipids reduces the risk and slows progression. Fenofibrate has now shown benefit in a dedicated randomised trial. Intravitreal anti-VEGF agents, including the bispecific antibody faricimab, and corticosteroid implants are the mainstay for vision-threatening disease, while several oral agents targeting individual pathways have not translated into clinical practice.
Conclusion: Effective pharmacotherapy of DR requires combining systemic risk-factor control with targeted intraocular therapy. Less invasive, longer-acting and neuroprotective strategies are the main unmet needs.
diabetic retinopathy; diabetic macular oedema; VEGF; anti-VEGF; fenofibrate; corticosteroids; faricimab; pharmacotherapy
Gajendra Jayant, Pooja Gourav, Omkar Rajput, Satyam Singh Jayant, Manoj Sharma. Pharmacology Role in Diabetic Retinopathy: A Review of Pathophysiology, Pharmacological Targets and Therapeutic Approaches. Indian Journal of Modern Research and Reviews. 2026; 4(10):39-44
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