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Glycobiology Advance Access published online on March 10, 2005
Glycobiology, doi:10.1093/glycob/cwi053
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org
Received December 22, 2004
Revised March 7, 2005
Accepted March 7, 2005

Article

Advanced Glycation End Products & RAGE: A Common Thread in Aging, Diabetes, Neurodegeneration & Inflammation

Ravichandran Ramasamy 1, Susan J. Vannucci 2, Shirley Shi Du Yan 3, Kevan Herold 4, Shi Fang Yan 1, and Ann Marie Schmidt 1*

1 Department of Surgery, Columbia University Medical Center, New York, New York 10032
2 Department of Pediatrics, Columbia University Medical Center, New York, New York 10032
3 Departments of Surgery & Pathology, Columbia University Medical Center, New York, New York 10032
4 Department of Medicine, Columbia University Medical Center, New York, New York 10032

* To whom correspondence should be addressed.
Ann Marie Schmidt, E-mail: ams11{at}columbia.edu


  Abstract

The products of nonenzymatic glycation and oxidation of proteins and lipids, the Advanced Glycation End Products (AGEs), accumulate in a wide variety of environments. AGEs may be generated rapidly or over long-periods of time stimulated by a range of distinct triggering mechanisms, thereby accounting for their roles in multiple settings and disease states. A critical property of AGEs is their ability to activate RAGE, a signal transduction receptor of the immunoglobulin superfamily. It is our hypothesis that due to such interaction, AGEs impart a potent impact in the tissues, stimulating processes linked to inflammation and its consequences. We hypothesize that AGEs cause perturbation in a diverse group of diseases, such as diabetes, inflammation, neurodegeneration and aging. Thus, we propose that targeting this pathway may represent a logical step in the prevention/treatment of the sequelae of these disorders.

Keywords: receptors, glucose, age, oxidative stress, injury.
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