Therapeutic Interruption of Advanced Glycation in Diabetic Nephropathy: Do All Roads Lead to Rome?
Authors: Sourris, Karly C.1; Forbes, Josephine M.1; Cooper, Mark E.1
Source: Annals of the New York Academy of Sciences, Volume 1126, Number 1, April 2008 , pp. 101-106(6)
Publisher: Blackwell Publishing
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Abstract:
A major common feature of the chemically disparate compounds that inhibit advanced glycation end product (AGE) accumulation or signaling is their ability to show end-organ protection in experimental models of diabetes complications. The mechanisms by which these AGE- lowering therapies confer their benefits remain unsolved. Is it the reduction in tissue AGE levels per se or the inhibition of downstream signal transduction (as has been described with the soluble receptor for AGE)? Possible modes of action that need to be investigated include the ability of some of these agents to stimulate antioxidant defenses, to lower cholesterol and other lipid levels, and to inhibit low-grade inflammation. To understand these novel mechanisms, further examination of the advanced glycation pathway and, in particular, the diverse action of these agents in ameliorating the development of diabetic complications is needed.Keywords: advanced glycation end products; diabetic nephropathy; reactive oxygen species; receptor for advanced glycation end products
Document Type: Research article
DOI: 10.1196/annals.1433.048
Affiliations: 1: JDRF Albert Einstein Centre for Diabetes Complications, Diabetes and Metabolism Division, Baker Heart Research Institute, Melbourne, Victoria, Australia
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