Therapeutic interruption of advanced glycation in diabetic nephropathy: Do all roads lead to Rome?

Karly C. Sourris, Josephine M. Forbes, Mark E. Cooper

Research output: Chapter in Book/Report/Conference proceedingConference PaperResearchpeer-review

16 Citations (Scopus)

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.

Original languageEnglish
Title of host publicationThe Maillard Reaction Recent Advances in Food and Biomedical Sciences
PublisherWiley-Blackwell
Pages101-106
Number of pages6
ISBN (Print)9781573317, 9789781573316
DOIs
Publication statusPublished - Apr 2008
Externally publishedYes

Publication series

NameAnnals of the New York Academy of Sciences
Volume1126
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Advanced glycation end products
  • Diabetic nephropathy
  • Reactive oxygen species
  • Receptor for advanced glycation end products

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