Diabetes and advanced glycation endproducts.
Bio-reactive advanced glycation endproducts (AGE) alter the structure and function of molecules in biological systems and increase oxidative stress. These adverse effects of both exogenous and endogenously derived AGE have been implicated in the pathogenesis of diabetic complications and changes associated with ageing including atherosclerosis, renal, eye and neurological disease. Specific AGE receptors and nonreceptor mechanisms contribute to these processes but also assist in the removal and degradation of AGE. The final disposal of AGE depends on renal clearance. Promising pharmacologic strategies to prevent AGE formation, reduce AGE toxicity, and/or inactivate AGE are under investigation.
Vlassara
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Department of Geriatrics, Mount Sinai School of Medicine, NY 10029, USA. helen.vlassara@mssm.edu
Palace
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MR
D000818:Animals; D003920:Diabetes Mellitus / Q000473:pathology / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000473:pathology / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000473:pathology / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000473:pathology / Q000503:physiopathology; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000473:pathology; D017127:Glycation End Products, Advanced / Q000502:physiology*; D006801:Humans; D007678:Kidney Glomerulus / Q000473:pathology; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000502:physiology
D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic