Receptor for advanced glycation endproducts and atherosclerosis: From basic mechanisms to clinical implications.

@article{citeulike:2222838, 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.}, address = {CNR, Institute of Clinical Physiology, San Cataldo Research Area, Via Moruzzi 1, 56124 Pisa, Italy.}, author = {Basta, Giuseppina }, citeulike-article-id = {2222838}, doi = {http://dx.doi.org/10.1016/j.atherosclerosis.2007.07.025}, journal = {Atherosclerosis}, keywords = {age, atherosclerosis}, month = {September}, posted-at = {2008-03-01 16:00:38}, priority = {2}, title = {Receptor for advanced glycation endproducts and atherosclerosis: From basic mechanisms to clinical implications.}, url = {http://dx.doi.org/10.1016/j.atherosclerosis.2007.07.025}, year = {2007} }

TY - JOUR ID - citeulike:2222838 L3 - citeulike-article-id:2222838 TI - Receptor for advanced glycation endproducts and atherosclerosis: From basic mechanisms to clinical implications. JF - Atherosclerosis AD - CNR, Institute of Clinical Physiology, San Cataldo Research Area, Via Moruzzi 1, 56124 Pisa, Italy. N2 - 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. KW - age KW - atherosclerosis AU - Basta, Giuseppina PY - 2007/09/07/ UR - http://dx.doi.org/10.1016/j.atherosclerosis.2007.07.025 ER -