Progenitor cell dysfunction: A key trigger for atherosclerotic inflammation

The availability of competent functional bone marrow-derived nucleated cells, such as endothelial progenitor cells (EPCs) capable of repair plays a determinant role in atherosclerosis genesis. In the presence of traditional risk factors for coronary artery disease, such as dyslipidemia, diabetes, hypertension renal failure, aging can be responsible for decreased availability of EPCs and the loss of arterial repair capacity. Although it is known that aging represents a formidable risk for coronary events, the mechanism underlying the effect of aging remains to be elucidated. We have proposed that the progressive depletion and/or functional impairment of bone marrow-derived EPCs might, at least in part, account for the effect of aging on atherosclerosis. Thus, the acquired inability of the bone marrow to provide progenitor cells capable of arterial repair in response to arterial injury might exacerbate the atherosclerotic inflammation, leading to arterial dysfunction.