Glycobiology Advance Access originally published online on March 10, 2005
Glycobiology 2005 15(7):16R-28R; doi:10.1093/glycob/cwi053
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Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation
2 Department of Surgery, Columbia University Medical Center, New York, NY 10032; 3 Department of Pediatrics, Columbia University Medical Center, New York, NY 10032; 4 Department of Pathology, Columbia University Medical Center, New York, NY 10032; and 5 Department of Medicine, Columbia University Medical Center, New York, NY 10032
1 To whom correspondence should be addressed; e-mail: ams11{at}columbia.edu
Received on December 22, 2004; revised on March 7, 2005; accepted on March 7, 2005
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 times 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 receptor for advanced glycation end products (RAGE), a signal transduction receptor of the immunoglobulin superfamily. It is our hypothesis that due to such interaction, AGEs impart a potent impact in 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.
Key words: age / glucose / injury / oxidative stress / receptors
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