Diabetic retinopathy (DR) has a complex pathogenesis which is impacted by a raft of systemic abnormalities
and tissue-specific alterations occurring in response to the diabetes milieu. Many pathogenic processes play key roles in
retinal damage in diabetic patients. One such pathway is the formation and accumulation of advanced glycation endproducts
(AGEs) and advanced lipoxidation end products (ALEs) which are relevant modifications with roles in the initiation
and progression of pathology. In this review, AGE/ALE formation in the diabetic retina is discussed alongside their impact
on retinal cell function. In addition, various inhibitors of the AGE-RAGE system and their therapeutic utility for DR
will also be evaluated.
Keywords: Diabetic retinopathy, advanced glycation end product, advanced lipoxidation end product, receptor for advanced
glycation endproduct, inflammation, oxidative stress, inhibitor, fusion protein.
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