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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/74048
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dc.contributor.authorMinicucci, Marcos Ferreira-
dc.contributor.authorGaiolla, Paula Schmidt Azevedo-
dc.contributor.authorPolegato, Bertha Furlan-
dc.contributor.authorPaiva, Sergio A.R.-
dc.contributor.authorZornoff, Leonardo Antonio Mamede-
dc.date.accessioned2014-05-27T11:27:25Z-
dc.date.accessioned2016-10-25T18:40:36Z-
dc.date.available2014-05-27T11:27:25Z-
dc.date.available2016-10-25T18:40:36Z-
dc.date.issued2012-12-04-
dc.identifierhttp://dx.doi.org/10.2174/187152812803589958-
dc.identifier.citationInflammation and Allergy - Drug Targets, v. 11, n. 6, p. 442-447, 2012.-
dc.identifier.issn1871-5281-
dc.identifier.urihttp://hdl.handle.net/11449/74048-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/74048-
dc.description.abstractCardiac 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.en
dc.format.extent442-447-
dc.language.isoeng-
dc.sourceScopus-
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 mechanismsen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.description.affiliationDepartment of Internal Medicine Botucatu Medical School UNESP - University of Estadual Paulista, Rubião Júnior s/n, Botucatu, SP, CEP: 18618-000-
dc.description.affiliationUnespDepartment of Internal Medicine Botucatu Medical School UNESP - University of Estadual Paulista, Rubião Júnior s/n, Botucatu, SP, CEP: 18618-000-
dc.identifier.doi10.2174/187152812803589958-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofInflammation and Allergy - Drug Targets-
dc.identifier.scopus2-s2.0-84870257839-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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