Smoking and endothelial progenitor cells: a revision of literature.
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.
Di Stefano
Rossella
R
Cardiac, Thoracic and Vascular Department, University of Pisa, Via Paradisa 2, 56124 Pisa, Italy. r.distefano@ao-pisa.toscana.it
Barsotti
Maria Chiara
MC
Felice
Francesca
F
Magera
Angela
A
Lekakis
John
J
Leone
Aurelio
A
Balbarini
Alberto
A
D000818:Animals; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology*; D006412:Hematopoietic Stem Cells / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D012307:Risk Factors; D015398:Signal Transduction / Q000502:physiology; D012907:Smoking / Q000009:adverse effects / Q000378:metabolism / Q000473:pathology*; D014028:Tobacco Smoke Pollution / Q000009:adverse effects
D014028:Tobacco Smoke Pollution