Background C-reactive protein (CRP), the prototypic marker of inflammation, has been shown to be an independent predictor of atherosclerosis.CRP can regulate receptor for advanced glycation end-products (RAGE) expression in endothelial progenitor cells (EPCs).Endothelial nitric oxide synthase (eNOS) deficiency is a pivotal event in atherogenesis.It is believed that decreased eNOS bioactivity occurs early in atherogenesis.Therefore, we tested the hypothesis that CRP can alter eNOS expression and promote apoptosis in EPCs through RAGE.