http://www.cnr.it/ontology/cnr/individuo/prodotto/ID24029
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
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Pagina inizio
- Pagina fine
- 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
- 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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