Several interactive and mutually perpetuating abnormal biochemical pathways, such as protein kinase C (PKC) activation, augmented polyol pathway, and non-enzymatic glycation, may be activated as a result of sustained hyperglycemia in diabetes. These abnormal pathways may in turn influence several vasoactive factors, which are probably instrumental in the production of functional and morphological changes in the retina in diabetes. The vasoactive factors such as endothelins, nitric oxide, vascular endothelial growth factors, etc., are of importance in mediating functional and structural alterations in early diabetic retinopathy. Intricate and interactive regulatory mechanism(s) among these factors may control ultimate availability of these molecules to produce biologically significant effects. A better understanding of these factors and their interactions would aid the development of adjuvant therapies for the treatment of diabetic retinopathy.
Copyright 2000 John Wiley & Sons, Ltd.