Abstract
Active and passive exposure to cigarette smoke (CS) increases the risk of, and has deleterious effects in, ischemic heart disease. Exposure to CS increases infarct size in experimental models of coronary occlusion and reperfusion. Among many possible mechanisms for these deleterious effects in intact animals and humans three have more substantial evidence: 1) functional alterations of endothelial cells, neutrophils and platelets; 2) impaired mitochondrial function and energy metabolism caused by toxins in CS, including oxidative free radicals; 3) increased arterial stiffness and vulnerability of the atherosclerotic plaque. In addition to the various pro-mitogenic, carcinogenic and apoptotic pathways thought to be affected and upregulated by CS, a direct necrotic action on cardiomyocytes is also believed to exist. Many, if not all, of these alterations are caused by oxidative stress, either as a direct consequence of inhalation of free radicals, or by induction from the vast range of chemicals present in both the gas and solid phase of tobacco smoke. Here, some of the proposed mechanisms will be reviewed and their impact on the cardiomyocytes and peripheral vasculature discussed.
Keywords: Oxidative stress, smoking, cardiomyocyte, endothelium
Current Pharmaceutical Design
Title: Adverse Effects of Cigarette Smoke and Induction of Oxidative Stress in Cardiomyocytes and Vascular Endothelium
Volume: 16 Issue: 23
Author(s): Anabel Varela Carver, Howard Parker, Christina Kleinert and Ornella Rimoldi
Affiliation:
Keywords: Oxidative stress, smoking, cardiomyocyte, endothelium
Abstract: Active and passive exposure to cigarette smoke (CS) increases the risk of, and has deleterious effects in, ischemic heart disease. Exposure to CS increases infarct size in experimental models of coronary occlusion and reperfusion. Among many possible mechanisms for these deleterious effects in intact animals and humans three have more substantial evidence: 1) functional alterations of endothelial cells, neutrophils and platelets; 2) impaired mitochondrial function and energy metabolism caused by toxins in CS, including oxidative free radicals; 3) increased arterial stiffness and vulnerability of the atherosclerotic plaque. In addition to the various pro-mitogenic, carcinogenic and apoptotic pathways thought to be affected and upregulated by CS, a direct necrotic action on cardiomyocytes is also believed to exist. Many, if not all, of these alterations are caused by oxidative stress, either as a direct consequence of inhalation of free radicals, or by induction from the vast range of chemicals present in both the gas and solid phase of tobacco smoke. Here, some of the proposed mechanisms will be reviewed and their impact on the cardiomyocytes and peripheral vasculature discussed.
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Cite this article as:
Varela Carver Anabel, Parker Howard, Kleinert Christina and Rimoldi Ornella, Adverse Effects of Cigarette Smoke and Induction of Oxidative Stress in Cardiomyocytes and Vascular Endothelium, Current Pharmaceutical Design 2010; 16 (23) . https://dx.doi.org/10.2174/138161210792062830
DOI https://dx.doi.org/10.2174/138161210792062830 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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