Circulating endothelial progenitor cells as novel biological determinants of vascular function and risk.

Endothelial progenitor cells (EPCs) are found in circulating mononuclear cells, bone marrow and cord blood, and have been shown to incorporate into areas of postnatal neovascularization stimulated by either ischemia or endothelial denudation. Endothelial cell injury is a hallmark of atherosclerotic plaque development triggered by a variety of cardiovascular risk factors, and the magnitude of endothelial dysfunction appears to be an independent predictor of cardiovascular risk. Several investigations have discovered that circulating levels of EPCs are diminished in individuals with cardiovascular risk factors which raises the possibility that this may contribute to endothelial dysfunction by impairing endothelial repair. In a study of adult men, it was found that the circulating EPC count was reduced in patients with multiple cardiovascular risk factors. Moreover, endothelial dysfunction was strongly correlated with EPC counts, such that subjects with risk factors developed endothelial dysfunction only if the EPC counts were low. EPCs of subjects with endothelial dysfunction were more senescent compared with an age-matched group without risk factors. These and other recent observations from experimental studies raise the possibility that vascular disease and dysfunction occur where injury is inflicted by exposure to risk factors in a setting of impaired repair capacity due to reduced availability of EPCs.