Open Access
Oxidative stress and accelerated vascular aging: implications for cigarette smoking
Anna Csiszar1,Andrej Podlutsky1,Michael S Wolin1,Gyorgy Losonczy1,Pal Pacher1,Zoltan Ungvari1
Department of Physiology, New York Medical College, Valhalla, NY 10595, USA
DOI: 10.2741/3440 Volume 14 Issue 8, pp.3128-3144
Published: 01 January 2009
(This article belongs to the Special Issue Nitric oxide, superoxide and peroxynitrite in cardiovascular diseases)

Cigarette smoking is the major cause of preventable morbidity and mortality in the United States and constitutes a major risk factor for atherosclerotic vascular disease, including coronary artery disease and stroke. Increasing evidence supports the hypothesis that oxidative stress and inflammation provide the pathophysiological link between cigarette smoking and CAD. Previous studies have shown that cigarette smoke activates leukocytes to release reactive oxygen and nitrogen species (ROS/RNS) and secrete pro-inflammatory cytokines, increases the adherence of monocytes to the endothelium and elicits airway inflammation. Here we present an overview of the direct effects of water-soluble cigarette smoke constituents on endothelial function, vascular ROS production and inflammatory gene expression. The potential pathogenetic role of peroxynitrite formation, and downstream mechanisms including poly(ADP-ribose) polymerase (PARP) activation in cardiovascular complications in smokers are also discussed.

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Anna Csiszar, Andrej Podlutsky, Michael S Wolin, Gyorgy Losonczy, Pal Pacher, Zoltan Ungvari. Oxidative stress and accelerated vascular aging: implications for cigarette smoking. Frontiers in Bioscience-Landmark. 2009. 14(8); 3128-3144.