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Use este identificador para citar o ir al link de este elemento: http://hdl.handle.net/1843/51225
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Campo DCValorIdioma
dc.creatorMichelle Adriane Amantéa Sugimotopt_BR
dc.creatorLirlândia Pires de Sousapt_BR
dc.creatorVanessa Pinhopt_BR
dc.creatorMauro Perrettipt_BR
dc.creatorMauro Martins Teixeirapt_BR
dc.date.accessioned2023-03-24T21:09:20Z-
dc.date.available2023-03-24T21:09:20Z-
dc.date.issued2016-04-26-
dc.citation.volume7pt_BR
dc.citation.spage1pt_BR
dc.citation.epage18pt_BR
dc.identifier.doi10.3389/fimmu.2016.00160pt_BR
dc.identifier.issn16643224pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/51225-
dc.description.resumoAn effective resolution program may be able to prevent the progression from non-resolving acute inflammation to persistent chronic inflammation. It has now become evident that coordinated resolution programs initiate shortly after inflammatory responses begin. In this context, several mechanisms provide the fine-tuning of inflammation and create a favorable environment for the resolution phase to take place and for homeostasis to return. In this review, we focus on the events required for an effective transition from the proinflammatory phase to the onset and establishment of resolution. We suggest that several mediators that promote the inflammatory phase of inflammation can simultaneously initiate a program for active resolution. Indeed, several events enact a decrease in the local chemokine concentration, a reduction which is essential to inhibit further infiltration of neutrophils into the tissue. Interestingly, although neutrophils are cells that characteristically participate in the active phase of inflammation, they also contribute to the onset of resolution. Further understanding of the molecular mechanisms that initiate resolution may be instrumental to develop pro-resolution strategies to treat complex chronic inflammatory diseases, in humans. The efforts to develop strategies based on resolution of inflammation have shaped a new area of pharmacology referred to as “resolution pharmacology.”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.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentFAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICASpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofFrontiers in Immunology-
dc.rightsAcesso Abertopt_BR
dc.subjectResolutionpt_BR
dc.subjectChemokine depletionpt_BR
dc.subjectEicosanoidspt_BR
dc.subjectPro-resolving mediatorspt_BR
dc.subjectTissue homeostasispt_BR
dc.subject.otherInflamaçãopt_BR
dc.titleResolution of inflammation: what controls its onset?pt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.frontiersin.org/articles/10.3389/fimmu.2016.00160/fullpt_BR
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