Diabetic retinopathy is a major cause of vision impairment and blindness and represents a significant health
burden throughout the world. There is considerable interest in developing new treatments that retard the progression of
diabetic retinopathy from its early to proliferative stages. It could be argued that the absence of an ideal therapy for
diabetic retinopathy comes from an incomplete understanding about the biochemical mechanisms that underlie this
disease, and their precise impact on specific retinal cell populations. Findings from pre-clinical and clinical studies
indicate that both the renin-angiotensin system (RAS) and advanced glycation end-products (AGEs) influence various
aspects of diabetic retinopathy. Of interest is growing evidence of cross-talk between the RAS and AGEs pathways. This
review will discuss the role of both the RAS and AGEs in diabetic retinopathy, and how the identification of interactions
between the two pathways may have implications for the development of new treatment strategies.
Keywords: Advanced glycation end-products, diabetic retinopathy, glyoxolase I, renin-angiotensin system.
Rights & PermissionsPrintExport