Smoking and Endothelial Progenitor Cells: A Revision of Literature

被引：24

作者：

Di Stefano, Rossella ^{[1
,2
]}

Barsotti, Maria Chiara ^{[1
]}

Felice, Francesca ^{[1
]}

Magera, Angela ^{[1
]}

Lekakis, John ^{[4
]}

Leone, Aurelio ^{[3
]}

Balbarini, Alberto ^{[1
,2
]}

机构：

[1] Univ Pisa, Cardiac Thorac & Vasc Dept, Cardiovasc Res Lab, I-56124 Pisa, Italy

[2] Univ Pisa, Angiol Unit, I-56124 Pisa, Italy

[3] Royal Soc Promot Hlth, London, England

[4] Alexandra Univ Hosp, Dept Cardiol, Athens, Greece

来源：

CURRENT PHARMACEUTICAL DESIGN | 2010年 / 16卷 / 23期

关键词：

Smoking; endothelial progenitor cells; nitric oxide; nicotine; NITRIC-OXIDE SYNTHASE; POLYCYCLIC AROMATIC-HYDROCARBONS; CARDIOVASCULAR RISK-FACTORS; PASSIVE SMOKING; CIGARETTE-SMOKING; PERIPHERAL-BLOOD; SECONDHAND SMOKE; TEA CONSUMPTION; CARBON-MONOXIDE; 2ND-HAND SMOKE;

D O I：

10.2174/138161210792062939

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Accumulating evidence indicates that circulating endothelial progenitor cells (EPCs) derived from bone marrow contribute to reendothelialization of injured 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.

引用

页码：2559 / 2566

页数：8

共 96 条

[41] Short-term passive smoking causes endothelial dysfunction via oxidative stress in nonsmokers [J].