Publication:

Current perspectives on the pathogenesis, molecular pathways, and therapeutic targets in diabetic retinopathy

Diabetic retinopathy (DR) is a serious sight-threatening complication that occurs due to constant hyperglycemia. It is the most common and leading cause of vision impairment worldwide. The development and progression of DR involve a complex network of genetic and environmental factors. Vascular inflammatory pathways, oxidative stress and epigenetic modifications have been linked to the development of diabetic mediated retinopathy. Candidate gene studies have implicated variants in genes involved in glucose metabolism such as (ALR2), vascular regulation (VEGF) are closely associated with DR susceptibility. Hyperglycemia triggers several factors such as polyol pathway, advanced glycation end-products (AGEs) formation, activation of protein kinase C (PKC), dysregulation of the renin-angiotensin system (RAS). These pathways collectively induce oxidative stress, inflammation, vascular dysfunction and pathological angiogenesis that further intensify microvascular lesions resulting in DR pathogenesis. Emerging therapeutic strategies present anti-VEGF agents, PKC inhibitors, and drugs modulating RAS system. In addition, targeted medicine based on genetic risk profiling and novel gene therapy approaches hold great promise in DR treatment. Further research integrating multi-omics data, gene-environment interactions, and precise translational studies are required for improving DR management and associated risk factor.