Abstract
Diabetic retinopathy (DR) remains a major cause of worldwide preventable blindness. The microvasculature of the retina responds to hyperglycemia through a number of biochemical changes, including activation of protein kinase C, increased advanced glycation end products formation, polyol pathway, and oxidative stress, and activation of the renin angiotensin system (RAS). There is an accumulating body of evidence that inflammation plays a prominent role in the pathogenesis of DR.