TY - JOUR
T1 - Progenitor cell dysfunction
T2 - A key trigger for atherosclerotic inflammation
AU - Goldschmidt-Clermont, Pascal J.
AU - Lam, Gregory
AU - Dong, Chunming
PY - 2004/10
Y1 - 2004/10
N2 - 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.
AB - 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.
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U2 - 10.1016/j.ddmec.2004.08.015
DO - 10.1016/j.ddmec.2004.08.015
M3 - Review article
AN - SCOPUS:23744473444
VL - 1
SP - 53
EP - 58
JO - Drug Discovery Today: Disease Mechanisms
JF - Drug Discovery Today: Disease Mechanisms
SN - 1740-6765
IS - 1
ER -