Lakhasly

DR is divided into two stages: non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR).Intravitreal administration of anti-VEGF agents is currently the mainstay of therapy for both early and advanced stages of DR. While the conventional laser therapy only provides stabilization of visual acuity, anti-VEGF therapy can result in visual improvement with less ocular adverse effects.However, according to the Diabetic Retinopathy Clinical Research Network (DRCR.net) study (Protocol I), >=3-line improvement in best-corrected visual acuity (BCVA) was achieved in only 29% of DME patients receiving two years of anti-VEGF treatment [2].The inadequate response to anti-VEGF may be associated with the involvement of other molecular pathways than VEGF during the pathogenesis of DR. Studies investigating the underlying mechanisms of DR are of great importance, which may provide potential targets for the development of new alternative treatments.NPDR represents the early stage of DR, wherein increased vascular permeability and capillary occlusion are two main observations in the retinal vasculature.

DR is divided into two stages: non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR). NPDR represents the early stage of DR, wherein increased vascular permeability and capillary occlusion are two main observations in the retinal vasculature. During this stage, retinal pathologies including microaneurysms, hemorrhages and hard exudates can be detected by fundus photography although the patients may be asymptomatic. PDR, a more advanced stage of DR, is characterized by neovascularization. During this stage, the patients may experience severe vision impairment when the new abnormal vessels bleed into the vitreous (vitreous hemorrhage) or when tractional retinal detachment is present. The most common cause of vision loss in patients with DR is diabetic macular edema (DME). DME is characterized by swelling or thickening of the macula due to sub- and intra-retinal accumulation of fluid in the macula triggered by the breakdown of the blood-retinal barrier (BRB) [1]. DME can occur at any stage of DR and cause distortion of visual images and a decrease in visual acuity. Current treatment strategies for DR aim at managing the microvascular complications, including intravitreal pharmacologic agents, laser photocoagulation and vitreous surgery. Intravitreal administration of anti-VEGF agents is currently the mainstay of therapy for both early and advanced stages of DR. While the conventional laser therapy only provides stabilization of visual acuity, anti-VEGF therapy can result in visual improvement with less ocular adverse effects. However, according to the Diabetic Retinopathy Clinical Research Network (DRCR.net) study (Protocol I), ≥3-line improvement in best-corrected visual acuity (BCVA) was achieved in only 29% of DME patients receiving two years of anti-VEGF treatment [2]. The inadequate response to anti-VEGF may be associated with the involvement of other molecular pathways than VEGF during the pathogenesis of DR. Studies investigating the underlying mechanisms of DR are of great importance, which may provide potential targets for the development of new alternative treatments. Here, we present a brief overview of current understanding of and new insights into the pathophysiology of DR. Novel therapeutic targets and potential pharmacological agents being tested in clinical trials are also discussed.