As is diabetes itself, diabetic angiopathy is a multi-factorial disease. Advanced glycation endproducts (AGE) cause vascular cell derangement characteristic of diabetes, and this is mainly mediated by their interaction with receptor for AGE (RAGE). When made diabetic, RAGE-overexpressing transgenic mice exhibited exacerbation of the indices of nephropathy, and this was prevented by the inhibition of AGE formation. On the other hand, RAGE-deficient animals showed amelioration of diabetic nephropathy. Accordingly, AGE and RAGE should be regarded as environmental and cellular accounts and as a potential therapeutic target for diabetic nephropathy. In effect, substances that inhibit the formation of AGE, break preformed AGE, change metabolic flows away from glycation, antagonize RAGE, and capture RAGE ligands have been proven as effective remedies against this life-threatening disease.
Keywords: iNOS transgenic mice, endothelial cells, aminoguanidine, RAGE gene, diabetic nephropathy
Semicarbazide-Sensitive Amine Oxidase: Current Status and Perspectives
Current Medicinal Chemistry Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 (LOX-1), a Relevant Target for Diabetic Vasculopathy?
Cardiovascular & Hematological Disorders-Drug Targets Targeting the Toll-System in Cardiovascular Sciences
Recent Patents on Inflammation & Allergy Drug Discovery