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Genetic disruption of NRF2 promotes the development of necroinflammation and liver fibrosis in a mouse model of HFE-hereditary hemochromatosis

2017-04Journal article Open access
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dc.contributor.authorDuarte, T.
dc.contributor.authorCaldas, C.
dc.contributor.authorSantos, A.
dc.contributor.authorSilva-Gomes, S.
dc.contributor.authorSantos-Gonçalves, A.
dc.contributor.authorMartins, M.
dc.contributor.authorPorto, G.
dc.contributor.authorLopes, J.
dc.date.accessioned2017-09-04T17:21:55Z
dc.date.available2017-09-04T17:21:55Z
dc.date.issued2017-04
dc.description.abstractIn hereditary hemochromatosis, iron deposition in the liver parenchyma may lead to fibrosis, cirrhosis and hepatocellular carcinoma. Most cases are ascribed to a common mutation in the HFE gene, but the extent of clinical expression is greatly influenced by the combined action of yet unidentified genetic and/or environmental modifying factors. In mice, transcription factor NRF2 is a critical determinant of hepatocyte viability during exposure to acute dietary iron overload. We evaluated if the genetic disruption of Nrf2 would prompt the development of liver damage in Hfe(-/-) mice (an established model of human HFE-hemochromatosis).pt_PT
dc.description.sponsorshipThis work was supported by National funds through Fundação para a Ciência e a Tecnologia/Ministério da Educação e Ciência (PTDC/SAU-FCF/101177/2008, PTDC/BIM-MET/0739/2012 and SFRH/BPD/108207/2015), by FEDER funds through the COMPETE – Operational Competitiveness Programme (FCOMP-01-0124-FEDER-011062 and FCOMP-01-0124-FEDER-028447) and Project Norte-01-0145-FEDER-000012, supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (FEDER), and by Reitoria da Universidade do Porto/Santander through PP-IJUP2011-122.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationRedox Biol. 2017 Apr;11:157-169pt_PT
dc.identifier.doi10.1016/j.redox.2016.11.013pt_PT
dc.identifier.issn2213-2317
dc.identifier.urihttp://hdl.handle.net/10400.16/2180
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.relationUnderstanding the contribution of iron overload in non-alcoholic fatty liver disease: identification of cellular players and potential molecular therapeutic targets
dc.relation.publisherversionhttp://www.sciencedirect.com/science/article/pii/S2213231716302749?via%3Dihubpt_PT
dc.subjectHepatocytept_PT
dc.subjectIronpt_PT
dc.subjectMacrophagept_PT
dc.subjectOxidative stresspt_PT
dc.subjectSideronecrosispt_PT
dc.titleGenetic disruption of NRF2 promotes the development of necroinflammation and liver fibrosis in a mouse model of HFE-hereditary hemochromatosispt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleUnderstanding the contribution of iron overload in non-alcoholic fatty liver disease: identification of cellular players and potential molecular therapeutic targets
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876-PPCDTI/PTDC%2FSAU-FCF%2F101177%2F2008/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876-PPCDTI/PTDC%2FBIM-MET%2F0739%2F2012/PT
oaire.citation.conferencePlaceNetherlandspt_PT
oaire.citation.endPage169pt_PT
oaire.citation.startPage157pt_PT
oaire.citation.titleRedox Biologypt_PT
oaire.citation.volume11pt_PT
oaire.fundingStream5876-PPCDTI
oaire.fundingStream5876-PPCDTI
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublication8066ec54-e63c-45df-8187-f59071f5493d
relation.isProjectOfPublication4d9607a3-ad4c-44e4-b05a-86e4dd4c5ddf
relation.isProjectOfPublication.latestForDiscovery4d9607a3-ad4c-44e4-b05a-86e4dd4c5ddf

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