IMR Press / FBL / Volume 14 / Issue 8 / DOI: 10.2741/3440

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Oxidative stress and accelerated vascular aging: implications for cigarette smoking
Show Less
1 Department of Physiology, New York Medical College, Valhalla, NY 10595
2 The Sam and Ann Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center, San Antonio, Texas 78245
3 Pulmonológiai Klinika, Semmelweis University, Budapest, Hungary
4 National Institutes of Health, National Institute on Alcohol Abuse & Alcoholism, Park Bldg., Rm. 445, 12420 Parklawn Drive, MSC-8115, Bethesda, MD 20892-8115
Front. Biosci. (Landmark Ed) 2009, 14(8), 3128–3144;
Published: 1 January 2009

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.

Back to top