Pathogenesis of Diabetic Retinopathy and Diabetic Macular Edema

The pathogenesis of diabetic retinopathy (DR) is complex and several vascular, inflammatory and neuronal mechanisms are involved. Diabetes causes a number of metabolic and physiologic abnormalities in the retina, but which of these abnormalities contribute to recognized features of DR is less clear. Angiogenesis and inflammation have been shown to be involved in the pathogenesis of this disease. Molecular mediators, acting in conjunction with metabolic pathways, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, leukostasis and ultimately diabetic macular edema (DME). The interactions, signalling events and feedback loops between the various molecular mediators and metabolic pathways are complicated and are not completely understood. The underlying mechanisms of DR and DME, on both microvascular and molecular levels, are discussed in this review.