Diabetic retinopathy is an ocular complication associated with the chronic endocrine disorder of diabetes mellitus. Angiogenesis is adjudged as a prime modulatory event in this complication. The formation of new blood vessels on the pre-existing vasculature gives rise to an abundance of anatomical and physiological alterations which ultimately results in vision loss. The drastic consequences of this complication prompt the obligation of developing effective therapies for its cure. The existing therapy mainly includes destructive techniques such as laser photocoagulation. Owing to the various drawbacks associated with this technique, there is a need to develop alternative therapies which could halt the progression of diabetic retinopathy without causing considerable damage to the retinal cells. One such possible alternative treatment being researched upon is the antiangiogenic therapy. Since angiogenesis is a critical event during the progression of this disorder, targeting this event may perhaps prove effective in its treatment. Amongst several antiangiogenic agents, thalidomide holds a reputable position due to its effectiveness in terminating angiogenesis during various pathological conditions. This review focuses on the diverse molecular mechanisms proposed to explain the antiangiogenic properties of thalidomide and their applicability in diabetic retinopathy.
Keywords: Angiopoietin-2; NF-kappa B; TNF-α; Thalidomide; VEGF; bFGF.
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