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 thei...

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Bibliographic Details
Published in:Glycobiology (Oxford) 2005-07, Vol.15 (7), p.16R-28R
Main Authors: Ramasamy, Ravichandran, Vannucci, Susan J., Yan, Shirley Shi Du, Herold, Kevan, Yan, Shi Fang, Schmidt, Ann Marie
Format: Article
Language:English
Subjects:
3-deoxyglucosone
3-DG
advanced glycation end product
age
Aging - physiology
aldose reductase
amyloid-beta peptide
Animals
carboxymethyl lysine
CML
dendritic cells
Diabetes Complications - physiopathology
dominant negative
endothelial cells
glucose
Glycation End Products, Advanced - physiology
Humans
Inflammation - physiopathology
injury
interleukin
Mice
mononuclear phagocytes
Neurodegenerative Diseases - physiopathology
nuclear factor
Oxidative Stress
RAGE
reactive oxygen species
Receptor for Advanced Glycation End Products
receptors
Receptors, Immunologic - physiology
ROS
SMC
smooth muscle cells
soluble RAGE
sRAGE
streptozotocin
stz
TLR
toll-like receptor
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Summary: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.
ISSN:0959-6658
1460-2423
DOI:10.1093/glycob/cwi053