Dengue virus infection induces inflammation and oxidative stress on the heart

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dc.creatorLucas Miranda Kangussu
dc.creatorMilene Alvarenga Rachid
dc.creatorRenan Pedra de Souza
dc.creatorCarlos Renato Tirapelli
dc.creatorRobson Augusto Souza dos Santos
dc.creatorJader dos Santos Cruz
dc.creatorMauro Martins Teixeira
dc.creatorDanielle da Glória de Souza
dc.creatorDaniella Bonaventura
dc.creatorVivian Vasconcelos Costa
dc.creatorVania Claudia Olivon
dc.creatorCelso Martins Queiroz Junior
dc.creatorAntônio Nei Santana Gondim
dc.creatorMarcos Barrouin Melo
dc.creatorDaniela Reis
dc.creatorNatália Nóbrega
dc.creatorNatália Araújo
dc.date.accessioned2023-07-14T22:22:57Z
dc.date.accessioned2025-09-09T01:07:16Z
dc.date.available2023-07-14T22:22:57Z
dc.date.issued2021
dc.identifier.doihttp://dx.doi.org/10.1136/heartjnl-2020-318912
dc.identifier.issn1355-6037
dc.identifier.urihttps://hdl.handle.net/1843/56319
dc.languagepor
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofHeart
dc.rightsAcesso Restrito
dc.subjectDengue
dc.subjectDoenças cardiacas
dc.subject.otherDengue virus (DENV)
dc.subject.otherCardiac dysfunction
dc.titleDengue virus infection induces inflammation and oxidative stress on the heart
dc.typeArtigo de periódico
local.citation.epage396
local.citation.spage388
local.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.
local.identifier.orcidhttps://orcid.org/0000-0003-3678-118X
local.identifier.orcidhttps://orcid.org/0000-0002-3142-6552
local.identifier.orcidhttps://orcid.org/0000-0002-9479-4432
local.identifier.orcidhttps://orcid.org/0000-0002-9779-733X
local.identifier.orcidhttps://orcid.org/0000-0001-5272-9651
local.identifier.orcidhttps://orcid.org/0000-0003-1365-2318
local.identifier.orcidhttps://orcid.org/0000-0002-6944-3008
local.identifier.orcidhttps://orcid.org/0000-0003-3432-0769
local.identifier.orcidhttps://orcid.org/0000-0001-5253-4918
local.identifier.orcidhttps://orcid.org/0000-0002-0175-642X
local.identifier.orcidhttps://orcid.org/0000-0001-6689-0972
local.identifier.orcidhttps://orcid.org/0000-0002-7884-7709
local.identifier.orcidhttps://orcid.org/0000-0002-2093-8480
local.identifier.orcidhttps://orcid.org/0000-0002-4524-0695
local.publisher.countryBrasil
local.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICA
local.publisher.departmentICB - DEPARTAMENTO DE MICROBIOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://heart.bmj.com/content/108/5/388

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