Journal
DIABETES
Volume 61, Issue 3, Pages 549-559Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db11-1120
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Funding
- Ministry of Education, Japan [18790619]
- University of South Carolina School of Medicine Center for Biomedical Research Excellence
- National Institute of Diabetes and Digestive and Kidney Diseases [DK071283, DK19971]
- U.S. Department of Energy (DOE) Office of Biological and Environmental Research [DE-AC06-76-RLO-1830]
- NephroGenex, Inc.
- Grants-in-Aid for Scientific Research [18790619] Funding Source: KAKEN
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This article outlines evidence that advanced glycation end product (AGE) inhibitors and breakers act primarily as chelators, inhibiting metal-catalyzed oxidation reactions that catalyze AGE formation. We then present evidence that chelation is the most likely mechanism by which ACE inhibitors, angiotensin receptor blockers, and aldose reductase inhibitors inhibit AGE formation in diabetes. Finally, we note several recent studies demonstrating therapeutic benefits of chelators for diabetic cardiovascular and renal disease. We conclude that chronic, low-dose chelation therapy deserves serious consideration as a clinical tool for prevention and treatment of diabetes complications. Diabetes 61:549-559, 2012
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