Objective: Recent studies have shown that visfatin enables to inhibit the endothelial cells aging via upregulating the expression of SIRT1.In coronary heart disease patients, endothelial progenitor cells (EPCs)have the impairment of proliferative, migratory capacity and network formation, suggesting that EPCs plays a critical role in genesis and development of atherosclerosis.Methods: EPCs were isolated by density gradient centrifugation from human cord blood mononuclear cells.After incubation of EPCs with different concentrations,we detected the capabilities of migration and tube formation in EPCs to judge the angiogenic effects of visfatin.Real time PCR was used to detect the expression of SIRT1 mRNA and western blot analysis was used to detect the protein level of SIRT1.We used a Quantitative telomerase detection kit to perform telomeric repeat amplification protocol (TRAP) assay.Senescent Cells Staining Kit was used to determine the senescence-associated β-galactosidase activity.Results: (1) 0.1 nM and 1 nM visfatin could enhance cell migration and tube formation reflecting angiogenic capability of EPCs.(2) 0.1 nM and l nM visfatin could upregulate the level of SIRT1 and telomerase activity (3) Senescence-associated β-galactosidase activity were significantly decreased with 0.1 nM visfatin.Conclusions: Visfatin at the physiological concentration could inhibit the EPCs aging via upregulating the expression of SIRT1.