Key result
Cigarette smoking, including active and second-hand smoke exposure, reduces the numbers and functional activity of circulating endothelial progenitor cells.
Why the study?
Does smoking exposure reduce the number and function of endothelial progenitor cells?
Does smoking exposure reduce the number and function of endothelial progenitor cells?
Answers are grounded in this paper and cite their sources.
This review highlights that active and second-hand smoke, as well as nicotine, significantly reduce the number and functional activity of circulating endothelial progenitor cells, contributing to cardiovascular risk.
Accumulating evidence indicates that circulating endothelial progenitor cells (EPCs) derived from bone marrow contribute to reendothelialization of injuried vessels as well as neo-vascularization of ischemic lesions in either a direct or an indirect way. Moreover, the number and/or the functional activity of EPCs are inversely correlated with risk factors for cardiovascular disease. Among the different risk factors, cigarette smoking is a major cause of reducing the numbers and function of circulating EPCs. This review is a revision of recent literature on EPC alteration associated with smoking. In particular, we show the recent observation on the effects of active and second hand smoke (SHS) exposure on EPC number and functional activity. This review also considers the effects of nicotine and other smoke compounds on EPC number and activity, in in vitro and in vivo models.
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Stefano et al. (2010) conducted a review in Cardiovascular disease risk factors (Smoking). Cigarette smoking (active and second-hand smoke) was evaluated on Endothelial progenitor cell (EPC) number and functional activity. Cigarette smoking, including active and second-hand smoke exposure, reduces the numbers and functional activity of circulating endothelial progenitor cells.
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