Aim To determine if circulating endothelial progenitor cells in patients with aortic dissection accelerated cell senescence via oxidative stress mechanism. Methods All patients with a symptom of chest pain were divided into control group and aortic dissection group according to the result of CT angiography. Endothelial progenitor cells were isolated and identified by flow cytometry analysis. The adhesion, migration and proliferation functions of endothelial progenitor cells were separately measured by the methods fibronectin adhesion, modified Boyden chamber and MTT array. Western blot was used to detect the protein level of p16INK4a and SIRT1. The level of intracellular reactive oxygen species was analyzed by the labeled H2DCF-DA method. Results The number of circulating CD34CD133KDR-positive endothelial progenitor cells in patients with aortic dissection decreased sharply(P<0.01)and cellular functions such as adhesion, migration and proliferation were damaged when compared with those in control group(P<0.05）. The protein level of the pro-senescent marker p16INK4a was found to upregulate significantly and meanwhile the expression of anti-senescent protein SIRT1 was decreased remarkably in the aortic dissection group(P<0.05）. The level of intracellular reactive oxygen species in patients with aortic dissection was increased severely(P<0.05）. Conclusions The accumulating intracellular reactive oxygen species were found to make those dysfunctions of circulating endothelial progenitor cells such as proliferation, adhesion and migration which probably accelerated endothelial progenitor cell senescence in patients with aortic dissection.