Diabetic retinopathy remains the leading vascular-associated cause of blindness throughout the world. Its treatment requires a multidisciplinary interventional approach at both systemic and local levels. Current management includes laser photocoagulation, intravitreal steroids, and anti-vascular endothelial growth factor (VEGF) treatment along with systemic blood sugar control. Anti-VEGF therapies, which are less destructive and safer than laser treatments, are being explored as primary therapy for the management of vision-threatening complications of diabetic retinopathy such as diabetic macular edema (DME). This review provides comprehensive information related to VEGF and describes its role in the pathogenesis of diabetic retinopathy, and in addition, examines the mechanisms of action for different antiangiogenic agents in relation to the management of this disease. Medline (Pubmed) searches were carried out with keywords “VEGF”, “diabetic retinopathy”, and “diabetes” without any year limitation to review relevant manuscripts used for this article.

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HQ-induced toxicity is concentration dependent in ARPE-19 and MIO-M1 cultures. MEM exerts protective effects against HQ-induced toxicity on human retinal pigment epithelial and Müller cells in vitro.

These studies indicate that two different breeds of pigmented rabbits exhibit different angiogenic responses to the same amount of both VEGF and bFGF. Florid retinal NV leading to hemorrhage, fibrovascular membrane formation, and traction retinal detachment occurred in the Dutch belt rabbits while tortuosity and dilatation of existing blood vessels with subsequent regression occurred in the NZW/Black satin cross animals. Such differences in the angio-genic response may be due to differences in the genetic background of these animals. If genetic heteriogeneity exists for angiogenic responses, then understanding the genetic role in the regulation of angiogenesis will lead to the design of more effective anti-angiogenic agents and can provide predictive outcomes of individual responses to therapy.

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