Cardiac remodeling induced by smoking: concepts, relevance, and potential mechanisms.
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.
Department of Internal Medicine, Botucatu Medical School, UNESP-University of Estadual Paulista, Botucatu, Brazil.
Marcos F
MF
Minicucci
Paula S
PS
Azevedo
Bertha F
BF
Polegato
Sergio A R
SA
Paiva
Leonardo A M
LA
Zornoff
D000818:Animals; D006801:Humans; D007249:Inflammation / Q000209:etiology; D020782:Matrix Metalloproteinases / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D012907:Smoking / Q000009:adverse effects*; D018487:Ventricular Dysfunction, Left / Q000209:etiology; D020257:Ventricular Remodeling
D009569:Nitric Oxide; D020928:Mitogen-Activated Protein Kinases; D020782:Matrix Metalloproteinases