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Inflammation & Allergy - Drug Targets (Discontinued)

Editor-in-Chief

ISSN (Print): 1871-5281
ISSN (Online): 2212-4055

Cardiac Remodeling Induced by Smoking: Concepts, Relevance, and Potential Mechanisms

Author(s): Marcos F. Minicucci, Paula S. Azevedo, Bertha F. Polegato, Sergio A.R. Paiva and Leonardo A.M. Zornoff

Volume 11, Issue 6, 2012

Page: [442 - 447] Pages: 6

DOI: 10.2174/187152812803589958

Price: $65

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Abstract

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.

Keywords: Matrix metalloproteinases, oxidative stress, tobacco smoke exposure, ventricular remodeling, Cardiac Remodeling, heart size, myocardial hypertrophy, ventricular dysfunction, hemodynamic, neurohormonal changes, oxidative stress, inflammation, mitogen-activated protein kinase activation


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