PUMA
Istituto di Fisiologia Clinica     
Basta G. Receptor for advanced glycation endproducts and atherosclerosis: from basic mechanisms to clinical implications. In: Atherosclerosis, vol. 196 (1) pp. 9 - 12. Elsevier, 2008.
 
 
Abstract
(English)
The receptor for advanced glycation endproducts (RAGE) is a member of the immunoglobulin superfamily of cell-surface molecules with a diverse repertoire of ligands. In the atherosclerotic milieu, three classes of RAGE ligands, i.e., products of non-enzymatic glycoxidation, S100 proteins and amphoterin, appear to drive receptor-mediated cellular activation and potentially, acceleration of vascular disease. The interaction of RAGE-ligands effectively modulates several steps of atherogenesis, triggering an inflammatory-proliferative process and furthermore, critically contributing to propagation of vascular perturbation, mainly in diabetes. RAGE has a circulating truncated variant isoform, soluble RAGE (sRAGE), corresponding to its extracellular domain only. By competing with cell-surface RAGE for ligand binding, sRAGE may contribute to the removal/neutralization of circulating ligands thus functioning as a decoy. The critical role of RAGE in the chronic vascular inflammation processes highlights this receptor-ligand axis as a possible and attractive candidate for therapeutic intervention to limit vascular damage and its associated clinical disorders.
URL: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T12-4PMJB3F-1&_user=3967543&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_version=1&_urlVersion=0&_userid=3967543&md5=266c138906e140060b7859e99e52ee55
DOI: 10.1016/j.atherosclerosis.2007.07.025
Subject Atherosclerosis
Amphoterin
S100 proteins
Receptor for advanced glycation endproducts


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