Recent advances in understanding the biochemical and molecular mechanism of diabetic retinopathy

Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes and remains a major cause of preventable blindness among adults at working age. DR involves an abnormal pathology of major retinal cells, including retinal pigment epithelium, microaneurysms, inter-retinal oedema, haemorrhage, exudates (hard exudates) and intraocular neovascularization. Hyperglycemia is the driving force for the development of diabetic retinopathy. The exact cause of diabetic nephropathy is unknown, but various postulated mechanisms are: hyperglycemia, advanced glycosylation products, activation of cytokines. In this review article, we have discussed a number of diabetes-induced metabolites such as glucose, advanced glycation end products, protein kinase C and oxidative stress and other related factors that are implicated in the pathophysiology of the DR. An understanding of the biochemical and molecular changes especially early in the DR may lead to new and effective therapies towards prevention and amelioration of DR.