1. Repositório Institucional da UFMG
  2. Publicações Científicas e Culturais
  3. Artigo de Periódico
Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/61210
Full metadata record
DC FieldValueLanguage
dc.creatorDiana Paola Gómez-Mendozapt_BR
dc.creatorFúlvia Dias Marquespt_BR
dc.creatorMarcella Nunes de Melo Bragapt_BR
dc.creatorRichard Remko Sprengerpt_BR
dc.creatorRubén Dario Sinisterra Millánpt_BR
dc.creatorFrank Kjeldsenpt_BR
dc.creatorRobson Augusto Souza dos Santospt_BR
dc.creatorThiago Verano-Bragapt_BR
dc.date.accessioned2023-11-21T20:13:07Z-
dc.date.available2023-11-21T20:13:07Z-
dc.date.issued2019-09-
dc.citation.volume208pt_BR
dc.identifier.doihttps://doi.org/10.1016/j.jprot.2019.103486pt_BR
dc.identifier.issn1876-7737pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/61210-
dc.description.resumoMyocardial infarction triggers cellular events that starts with the activation of inflammatory response and fibrogenic pathways involved in cardiac tissue remodeling. Angiotensin-(1–7) (Ang-(1–7)) is an endogenous heptapeptide from the renin-angiotensin system with a cardioprotective role due to its anti-inflammatory and anti-fibrotic activities in cardiac cells. Although the beneficial aspects of Ang-(1–7) in animal models of cardiac ischemia have been reported, the molecular events underlying Ang-(1–7) cardioprotective effect remains elusive. This study investigated the impact of oral treatment with Ang-(1–7) included in hydroxypropyl β-cyclodextrin (HPβCD/Ang-(1–7)) on the cardiac proteome dysregulation due to experimental myocardial infarction. Wistar male rats were submitted to experimental myocardial infarction and treated daily with HPβCD/Ang-(1–7) during 7 days or 60 days by gavage. Our results showed that HPβCD/Ang-(1–7) treatment ameliorates the post-infarction condition due to the modulation of proteins that initially favor the resolution of inflammation and mitochondrial dysfunction. Moreover, this study reported for the first time that Ang-(1–7) treatment after experimental myocardial infarction leads to the downregulation of the C-X-C chemokine receptor type 4 (CXCR4).pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Geraispt_BR
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.description.sponsorshipOutra Agênciapt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICApt_BR
dc.publisher.departmentICX - DEPARTAMENTO DE QUÍMICApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofJournal of Proteomicspt_BR
dc.rightsAcesso Restritopt_BR
dc.subjectAngiotensin-(1–7)pt_BR
dc.subjectAnti-inflammatorypt_BR
dc.subjectMyocardial infarctionpt_BR
dc.subjectProteomicspt_BR
dc.subjectCXCR4pt_BR
dc.subject.otherAngiotensinapt_BR
dc.subject.otherEnfarte do miocárdiopt_BR
dc.subject.otherAgentes antiinflamatóriospt_BR
dc.subject.otherCiclodextrinaspt_BR
dc.titleAngiotensin-(1-7) oral treatment after experimental myocardial infarction leads to downregulation of CXCR4pt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.sciencedirect.com/science/article/pii/S1874391919302581pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-3318-3539pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6174-8157pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-3947-1606pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-7656-1849pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-0785-2903pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7083-2588pt_BR
Appears in Collections:Artigo de Periódico

Files in This Item:
There are no files associated with this item.
Show simple item record


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.