The pathological role of the non-enzymatic modification of proteins by reducing sugars has become increasingly evident in various types of diseases [ 1 Rahbar S. Figarola J.L. Novel inhibitors of advanced glycation endproducts. Arch Biochem Biophys. 2003; 419: 63-79 Crossref PubMed Scopus (298) Google Scholar , 2 Yamagishi S. Imaizumi T. Diabetic vascular complications: pathophysiology, biochemical basis and potential therapeutic strategy. Curr Pharm Des. 2005; 11: 2279-2299 Crossref PubMed Scopus (429) Google Scholar ]. It is now well established that early glycation products undergo progressive modification over time in vivo to the formation of irreversible cross-links, after which these molecules are termed “advanced glycation end products (AGEs)” [ 1 Rahbar S. Figarola J.L. Novel inhibitors of advanced glycation endproducts. Arch Biochem Biophys. 2003; 419: 63-79 Crossref PubMed Scopus (298) Google Scholar , 2 Yamagishi S. Imaizumi T. Diabetic vascular complications: pathophysiology, biochemical basis and potential therapeutic strategy. Curr Pharm Des. 2005; 11: 2279-2299 Crossref PubMed Scopus (429) Google Scholar ]. There is accumulating evidence that AGEs and their receptor RAGE interaction are involved in cardiovascular disease, insulin resistance and diabetic complications [ 2 Yamagishi S. Imaizumi T. Diabetic vascular complications: pathophysiology, biochemical basis and potential therapeutic strategy. Curr Pharm Des. 2005; 11: 2279-2299 Crossref PubMed Scopus (429) Google Scholar , 3 Bierhaus A. Hofmann M.A. Ziegler R. Nawroth P.P. AGEs and their interaction with AGE-receptors in vascular disease and diabetes mellitus. I. The AGE concept. Cardiovasc Res. 1998; 37: 586-600 Crossref PubMed Scopus (501) Google Scholar , 4 Yan S.F. D'Agati V. Schmidt A.M. Ramasamy R. Receptor for advanced glycation endproducts (RAGE): a formidable force in the pathogenesis of the cardiovascular complications of diabetes & aging. Curr Mol Med. 2007; 7: 699-710 Crossref PubMed Scopus (114) Google Scholar ]. Moreover, administration of a recombinant soluble form of RAGE (sRAGE) has been shown to suppress the development and progression of atherosclerosis in diabetic apolipoprotein E-null mice [ [4] Yan S.F. D'Agati V. Schmidt A.M. Ramasamy R. Receptor for advanced glycation endproducts (RAGE): a formidable force in the pathogenesis of the cardiovascular complications of diabetes & aging. Curr Mol Med. 2007; 7: 699-710 Crossref PubMed Scopus (114) Google Scholar ]. These observations suggest that exogenously administered sRAGE may capture circulating AGEs by acting as a decoy receptor.