Cardiovascular remodeling induced by passive smoking

dc.contributor.authorMinicucci, Marcos Ferreira [UNESP]
dc.contributor.authorGaiolla, Paula Schmidt Azevedo [UNESP]
dc.contributor.authorPaiva, Sergio Alberto Rupp de [UNESP]
dc.contributor.authorZornoff, Leonardo Antonio Mamede [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:24:05Z
dc.date.available2014-05-27T11:24:05Z
dc.date.issued2009-12-01
dc.description.abstractCoronary heart disease (CHD) is the most common cause of death in many developed countries. The major risk factors for CHD are smoking, high blood pressure, diabetes, high cholesterol levels, and lack of physical activity. Importantly, passive smoke also increases the risk for CHD. The mechanisms involved in the effects of passive smoke in CHD are complex and include endothelial dysfunction, lipoprotein modification, increased inflammation and platelet activation. Recently, several studies have shown that exposure to tobacco smoke can result in cardiac remodeling and compromised cardiac function. Potential mechanisms for these alterations are neurohumoral activation, oxidative stress, and MAPK activation. Although the vascular effects of cigarette smoke exposure are well known, the effects of tobacco smoking on the heart have received less attention. Therefore, this review will focus on the recent findings as to the effects of passive smoking in acute and chronic phases of vascular and cardiac remodeling. © 2009 Bentham Science Publishers Ltd.en
dc.description.affiliationDepartment of Internal Medicine Botucatu Medical School UNESP - São Paulo State University, Botucatu, Sao Paulo
dc.description.affiliationUnespDepartment of Internal Medicine Botucatu Medical School UNESP - São Paulo State University, Botucatu, Sao Paulo
dc.format.extent334-339
dc.identifierhttp://dx.doi.org/10.2174/187152809790031289
dc.identifier.citationInflammation and Allergy - Drug Targets, v. 8, n. 5, p. 334-339, 2009.
dc.identifier.doi10.2174/187152809790031289
dc.identifier.issn1871-5281
dc.identifier.lattes5016839015394547
dc.identifier.lattes1213140801402647
dc.identifier.lattes7438704034471673
dc.identifier.orcid0000-0002-5843-6232
dc.identifier.scopus2-s2.0-74849118477
dc.identifier.urihttp://hdl.handle.net/11449/71345
dc.language.isoeng
dc.relation.ispartofInflammation and Allergy - Drug Targets
dc.relation.ispartofsjr0,649
dc.rights.accessRightsAcesso restrito
dc.sourceScopus
dc.subjectgelatinase A
dc.subjectgelatinase B
dc.subjectmitogen activated protein kinase
dc.subjectmitogen activated protein kinase 1
dc.subjectmitogen activated protein kinase 3
dc.subjecttobacco smoke
dc.subjectcardiovascular disease
dc.subjectcardiovascular remodeling
dc.subjectechocardiography
dc.subjectendothelium
dc.subjectenvironmental exposure
dc.subjecthuman
dc.subjectinflammation
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpassive smoking
dc.subjectreview
dc.subjectthrombocyte activation
dc.subjectvascular disease
dc.subjectAnimals
dc.subjectCoronary Disease
dc.subjectCoronary Vessels
dc.subjectHeart Ventricles
dc.subjectHumans
dc.subjectInflammation Mediators
dc.subjectMetalloproteases
dc.subjectPlatelet Activation
dc.subjectProtein Kinases
dc.subjectRisk Factors
dc.subjectTobacco
dc.subjectTobacco Smoke Pollution
dc.titleCardiovascular remodeling induced by passive smokingen
dc.typeResenha
dcterms.licensehttp://www.ingentaconnect.com/about/terms
unesp.author.lattes5016839015394547
unesp.author.lattes1213140801402647[2]
unesp.author.lattes7438704034471673
unesp.author.orcid0000-0002-5843-6232[2]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt
unesp.departmentClínica Médica - FMBpt

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