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Use este identificador para citar ou linkar para este item: http://hdl.handle.net/1843/56319
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Campo DCValorIdioma
dc.creatorLucas Miranda Kangussupt_BR
dc.creatorMilene Alvarenga Rachidpt_BR
dc.creatorRenan Pedra de Souzapt_BR
dc.creatorCarlos Renato Tirapellipt_BR
dc.creatorRobson Augusto Souza dos Santospt_BR
dc.creatorJader dos Santos Cruzpt_BR
dc.creatorMauro Martins Teixeirapt_BR
dc.creatorDanielle da Glória de Souzapt_BR
dc.creatorDaniella Bonaventurapt_BR
dc.creatorVivian Vasconcelos Costapt_BR
dc.creatorVania Claudia Olivonpt_BR
dc.creatorCelso Martins Queiroz Juniorpt_BR
dc.creatorAntônio Nei Santana Gondimpt_BR
dc.creatorMarcos Barrouin Melopt_BR
dc.creatorDaniela Reispt_BR
dc.creatorNatália Nóbregapt_BR
dc.creatorNatália Araújopt_BR
dc.date.accessioned2023-07-14T22:22:57Z-
dc.date.available2023-07-14T22:22:57Z-
dc.date.issued2021-
dc.citation.spage388pt_BR
dc.citation.epage396pt_BR
dc.identifier.doihttp://dx.doi.org/10.1136/heartjnl-2020-318912pt_BR
dc.identifier.issn1355-6037pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/56319-
dc.description.resumoObjective Dengue fever is one of the most important arboviral diseases in the world, and its severe forms are characterised by a broad spectrum of systemic and cardiovascular hallmarks. However, much remains to be elucidated regarding the pathogenesis triggered by Dengue virus (DENV) in the heart. Herein, we evaluated the cardiac outcomes unleashed by DENV infection and the possible mechanisms associated with these effects. Methods A model of an adapted DENV- 3 strain was used to infect male BALB/c mice to assess haemodynamic measurements and the functional, electrophysiological, inflammatory and oxidative parameters in the heart. Results DENV- 3 infection resulted in increased systemic inflammation and vascular permeability with consequent reduction of systolic blood pressure and increase in heart rate. These changes were accompanied by a decrease in the cardiac output and stroke volume, with a reduction trend in the left ventricular end- systolic and end- diastolic diameters and volumes. Also, there was a reduction trend in the calcium current density in the ventricular cardiomyocytes of DENV- 3 infected mice. Indeed, DENV- 3 infection led to leucocyte infiltration and production of inflammatory mediators in the heart, causing pericarditis and myocarditis. Moreover, increased reactive oxygen species generation and lipoperoxidation were also verified in the cardiac tissue of DENV- 3 infected mice. Conclusions DENV- 3 infection induced a marked cardiac dysfunction, which may be associated with inflammation, oxidative stress and electrophysiological changes in the heart. These findings provide new cardiac insights into the mechanisms involved in the pathogenesis triggered by DENV, contributing to the research of new therapeutic targets for clinical practice.pt_BR
dc.languageporpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE MICROBIOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofHeartpt_BR
dc.rightsAcesso Restritopt_BR
dc.subjectDengue virus (DENV)pt_BR
dc.subjectCardiac dysfunctionpt_BR
dc.subject.otherDenguept_BR
dc.subject.otherDoenças cardiacaspt_BR
dc.titleDengue virus infection induces inflammation and oxidative stress on the heartpt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://heart.bmj.com/content/108/5/388pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-3678-118Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-3142-6552pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9479-4432pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9779-733Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-5272-9651pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-1365-2318pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6944-3008pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-3432-0769pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-5253-4918pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-0175-642Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-6689-0972pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7884-7709pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-2093-8480pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-4524-0695pt_BR
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