Cardiac remodeling induced by smoking: Concepts, relevance, and potential mechanisms

dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorMinicucci, Marcos Ferreira
dc.creatorGaiolla, Paula Schmidt Azevedo
dc.creatorPolegato, Bertha Furlan
dc.creatorPaiva, Sergio A.R.
dc.creatorZornoff, Leonardo Antonio Mamede
dc.date2014-05-27T11:27:25Z
dc.date2016-10-25T18:40:36Z
dc.date2014-05-27T11:27:25Z
dc.date2016-10-25T18:40:36Z
dc.date2012-12-04
dc.date.accessioned2017-04-06T02:06:02Z
dc.date.available2017-04-06T02:06:02Z
dc.identifierInflammation and Allergy - Drug Targets, v. 11, n. 6, p. 442-447, 2012.
dc.identifier1871-5281
dc.identifierhttp://hdl.handle.net/11449/74048
dc.identifierhttp://acervodigital.unesp.br/handle/11449/74048
dc.identifier10.2174/187152812803589958
dc.identifier2-s2.0-84870257839
dc.identifierhttp://dx.doi.org/10.2174/187152812803589958
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/894823
dc.descriptionCardiac 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.
dc.languageeng
dc.relationInflammation and Allergy - Drug Targets
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectMatrix metalloproteinases
dc.subjectOxidative stress
dc.subjectTobacco smoke exposure
dc.subjectVentricular remodeling
dc.subjectacetylcysteine
dc.subjectadenosine triphosphate
dc.subjectbeta carotene
dc.subjectcalcium channel L type
dc.subjectcalcium ion
dc.subjectgamma interferon
dc.subjectgelatinase B
dc.subjectinterleukin 1
dc.subjectinterleukin 18
dc.subjectinterleukin 6
dc.subjectmitogen activated protein kinase
dc.subjectneurohormone
dc.subjectnicotine
dc.subjectnitric oxide
dc.subjectreactive oxygen metabolite
dc.subjecttaurine
dc.subjecttobacco smoke
dc.subjecttumor necrosis factor alpha
dc.subjectvitamin D
dc.subjectcalcium mobilization
dc.subjectcytokine production
dc.subjectenergy metabolism
dc.subjectexposure
dc.subjectheart disease
dc.subjectheart infarction
dc.subjectheart muscle contractility
dc.subjectheart size
dc.subjectheart ventricle failure
dc.subjectheart ventricle hypertrophy
dc.subjectheart ventricle remodeling
dc.subjecthemodynamic stress
dc.subjecthypoxemia
dc.subjectinflammation
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectrenin angiotensin aldosterone system
dc.subjectsmoking
dc.subjectsupplementation
dc.subjectAnimals
dc.subjectHumans
dc.subjectInflammation
dc.subjectMatrix Metalloproteinases
dc.subjectMitogen-Activated Protein Kinases
dc.subjectNitric Oxide
dc.subjectOxidative Stress
dc.subjectSmoking
dc.subjectVentricular Dysfunction, Left
dc.subjectVentricular Remodeling
dc.titleCardiac remodeling induced by smoking: Concepts, relevance, and potential mechanisms
dc.typeOtro


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