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Advanced glycation end products (AGEs) and receptor for AGE (RAGE)-mediated mechanism has been implicated in the pathogenesis of the vascular derangements.1–3 Yonekura et al recently identified a novel splice variant of RAGE that would serve as a decoy receptor, and named it endogenous secretory RAGE (esRAGE).4 esRAGE is secreted from expresser cells exemplified by vascular endothelial cells and is able to captures RAGE ligands extracellularly, thereby protecting cells from AGE-induced injury.4 Recently, we reported that type 1 diabetic patients with high serum esRAGE levels were resistant to developing early retinal complications than those with low esRAGE levels.5 Moreover, plasma esRAGE is found to be a novel biomarker and a potential protective factor in metabolic syndrome and atherosclerosis.6 It is thus expected that esRAGE plays a protective role in the development of diabetic vascular complications. The balance or imbalance between RAGE ligand and esRAGE levels may be a …

Endogenous Secretory Receptor for Advanced Glycation Endproducts Levels Are Correlated With Serum Pentosidine and CML in Patients With Type 1 Diabetes