Cardiac remodeling induced by smoking: Concepts, relevance, and potential mechanisms
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Bentham Science Publishers
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Cardiac or ventricular remodeling is characterized by molecular, cellular, and interstitial alterations that lead to changes in heart size, mass, geometry and function in response to a given insult. Currently, tobacco smoke exposure is recognized as one of these insults. Indeed, tobacco smoke exposure induces the enlargement of the left-sided cardiac chambers, myocardial hypertrophy, and ventricular dysfunction. Potential mechanisms for these alterations include hemodynamic and neurohormonal changes, oxidative stress, inflammation, nitric oxide bioavailability, matrix metalloproteinases and mitogen-activated protein kinase activation. This review will focus on the concepts, relevance, and potential mechanisms of cardiac remodeling induced by tobacco smoke. © 2012 Bentham Science Publishers.
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Matrix metalloproteinases Oxidative stress Tobacco smoke exposure Ventricular remodeling acetylcysteine adenosine triphosphate beta carotene calcium channel L type calcium ion gamma interferon gelatinase B interleukin 1 interleukin 18 interleukin 6 mitogen activated protein kinase neurohormone nicotine nitric oxide reactive oxygen metabolite taurine tobacco smoke tumor necrosis factor alpha vitamin D calcium mobilization cytokine production energy metabolism exposure heart disease heart infarction heart muscle contractility heart size heart ventricle failure heart ventricle hypertrophy heart ventricle remodeling hemodynamic stress hypoxemia inflammation nonhuman oxidative stress renin angiotensin aldosterone system smoking supplementation Animals Humans Inflammation Matrix Metalloproteinases Mitogen-Activated Protein Kinases Nitric Oxide Oxidative Stress Smoking Ventricular Dysfunction, Left Ventricular Remodeling
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Inflammation and Allergy - Drug Targets, v. 11, n. 6, p. 442-447, 2012.
