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dc.contributor.authorMinicucci, Marcos Ferreira-
dc.contributor.authorGaiolla, Paula Schmidt Azevedo-
dc.contributor.authorPaiva, Sergio Alberto Rupp de-
dc.contributor.authorZornoff, Leonardo Antonio Mamede-
dc.date.accessioned2014-05-27T11:24:05Z-
dc.date.accessioned2016-10-25T18:27:51Z-
dc.date.available2014-05-27T11:24:05Z-
dc.date.available2016-10-25T18:27:51Z-
dc.date.issued2009-12-01-
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.issn1871-5281-
dc.identifier.urihttp://hdl.handle.net/11449/71345-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/71345-
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.format.extent334-339-
dc.language.isoeng-
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.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
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.identifier.doi10.2174/187152809790031289-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofInflammation and Allergy - Drug Targets-
dc.identifier.scopus2-s2.0-74849118477-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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