Receptor for advanced glycation endproducts and atherosclerosis: from basic mechanisms to clinical implications (Articolo in rivista)

Type
Label
  • Receptor for advanced glycation endproducts and atherosclerosis: from basic mechanisms to clinical implications (Articolo in rivista) (literal)
Anno
  • 2008-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/j.atherosclerosis.2007.07.025 (literal)
Alternative label
  • Basta G. (2008)
    Receptor for advanced glycation endproducts and atherosclerosis: from basic mechanisms to clinical implications
    in Atherosclerosis (Amst.)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Basta G. (literal)
Pagina inizio
  • 9 (literal)
Pagina fine
  • 12 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
  • http://dx.doi.org/10.1016/j.atherosclerosis.2007.07.025 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 196 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
  • In: Atherosclerosis, vol. 196 (1) pp. 9 - 12. Elsevier, 2008. (literal)
Note
  • PubMe (literal)
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • CNR, Institute of Clinical Physiology, Pisa, Italy (literal)
Titolo
  • Receptor for advanced glycation endproducts and atherosclerosis: from basic mechanisms to clinical implications (literal)
Abstract
  • 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. (literal)
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