Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation.
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.
Ramasamy
Ravichandran
R
Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA.
Vannucci
Susan J
SJ
Yan
Shirley Shi Du
SS
Herold
Kevan
K
Yan
Shi Fang
SF
Schmidt
Ann Marie
AM
D000375:Aging / Q000502:physiology*; D000818:Animals; D048909:Diabetes Complications / Q000503:physiopathology*; D017127:Glycation End Products, Advanced / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D051379:Mice; D019636:Neurodegenerative Diseases / Q000503:physiopathology*; D018384:Oxidative Stress; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000502:physiology*
D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic