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

Atherosclerosis. 2008 Jan;196(1):9-21. doi: 10.1016/j.atherosclerosis.2007.07.025. Epub 2007 Sep 10.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis / immunology
  • Atherosclerosis / physiopathology*
  • Disease Models, Animal
  • Glycation End Products, Advanced / physiology
  • HMGB1 Protein
  • Humans
  • Inflammation / physiopathology*
  • Mice
  • Oxidative Stress
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / physiology*
  • S100 Proteins / physiology


  • Glycation End Products, Advanced
  • HMGB1 Protein
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic
  • S100 Proteins