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Advanced glycation: how are we progressing to combat this web of sugar anomalies in diabetic nephropathy
Josephine M Forbes1, Vicki Thallas-Bonke, Mark E Cooper
1Danielle Alberti Memorial Centre for Diabetes Complications, Wynn Domain, Vascular Division, Baker Heart Research Institute, Melbourne, Victoria 8008, Australia. Josephine.forbes@baker.edu.au
Abstract:
Advanced glycation end products (AGEs) in diabetic nephropathy have been extensively researched over the last decade and are now firmly established as major players in this disease. The enigma remains the search for the ideal AGE inhibition therapy, which is a great challenge in the context of the structural diversity inherent to AGE chemistry. Certainly, there is a requirement to standardize measurements of circulating and tissue levels of AGEs and to characterize the pathogenic potential of specific AGE moieties. In order to develop more effective, targeted approaches to combat diabetic nephropathy, the mechanisms of action of selective AGE inhibitors and the inter-relationships of advanced glycation with other pathogenic pathways must be addressed.
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