Biochemical and molecular mechanisms of diabetic retinopathy

Abstract

Diabetic retinopathy is one of the most common devastating complications of diabetes. Currently there a are no accepted drug treatments for diabetic retinopathy and laser therapy is the most accepted treatment option. Biochemical and physiological changes that occur very early in the retina of diabetic patients are the major signaling determinants of future damage to the retina. However, drug treatment for diabetic retir nopathy that will specifically ameliorate biochemical defects, is still only at an experimental stage. Research during the past few decades has provided ample evidence that hyperglycaemia is one of the main factors driving the onset and progression of diabetic retinopathy. Furthermore, hyperglycaemia-induced events regulate a variety of cellular signals including the stimulation of growth factors that are implicated in retinopathy. It is possible that in the future, novel therapeutic measures may emerge for the treatment of diabetic retinopathy. In order to discover anti-permeability and anti-angiogenic compounds, a more comprehensive understanding of the mechanisms governing the vascularization of the retina is required. Some of the experimental approaches currently under investigation, such as protein kinase C inhibitors, VEGF inhibitors, pigment epithelium-derived factor, and many others may prove useful as new therapeutic approaches in the treatment of various stages of diabetic retinopathy. Significant efforts continue to be directed toward the evaluation of the mechanisms underlying diabetic retinopathy in order to achieve newer and better therapies for this potentially preventable cause of blindness.