Receptor for AGE (RAGE): signaling mechanisms in the pathogenesis of diabetes and its complications
Article first published online: 23 DEC 2011
© 2011 New York Academy of Sciences.
Annals of the New York Academy of Sciences
Volume 1243, The Year in Diabetes and Obesity pages 88–102, December 2011
How to Cite
Ramasamy, R., Yan, S. F. and Schmidt, A. M. (2011), Receptor for AGE (RAGE): signaling mechanisms in the pathogenesis of diabetes and its complications. Annals of the New York Academy of Sciences, 1243: 88–102. doi: 10.1111/j.1749-6632.2011.06320.x
- Issue published online: 23 DEC 2011
- Article first published online: 23 DEC 2011
- signal transduction
The receptor for advanced glycation endproducts (RAGE) was first described as a signal transduction receptor for advanced glycation endproducts (AGEs), the products of nonenzymatic glycation and oxidation of proteins and lipids that accumulate in diabetes and in inflammatory foci. The discovery that RAGE was a receptor for inflammatory S100/calgranulins and high mobility group box 1 (HMGB1) set the stage for linking RAGE to both the consequences and causes of types 1 and 2 diabetes. Recent discoveries regarding the structure of RAGE as well as novel intracellular binding partner interactions advance our understanding of the mechanisms by which RAGE evokes pathological consequences and underscore strategies by which antagonism of RAGE in the clinic may be realized. Finally, recent data tracking RAGE in the clinic suggest that levels of soluble RAGEs and polymorphisms in the gene encoding RAGE may hold promise for the identification of patients who are vulnerable to the complications of diabetes and/or are receptive to therapeutic interventions designed to prevent and reverse the damage inflicted by chronic hyperglycemia, irrespective of its etiology.