Utilize este identificador para referenciar este registo: http://hdl.handle.net/10362/21941
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dc.contributor.authorDuarte, Nádia-
dc.contributor.authorCoelho, Inês C-
dc.contributor.authorPatarrão, Rita S.-
dc.contributor.authorAlmeida, Joana I-
dc.contributor.authorGonçalves, Carlos Penha-
dc.contributor.authorMacedo, M. Paula-
dc.date.accessioned2017-07-13T22:01:04Z-
dc.date.available2017-07-13T22:01:04Z-
dc.date.issued2015-
dc.identifier.issn2314-6133-
dc.identifier.otherPURE: 489655-
dc.identifier.otherPURE UUID: 80bcb4e4-663d-4e19-a6e0-bef38b916aa9-
dc.identifier.otherresearchoutputwizard: 51511-
dc.identifier.otherPubMed: 26090470-
dc.identifier.otherWOS: 000355524600001-
dc.identifier.otherScopus: 84930959966-
dc.identifier.urihttp://hdl.handle.net/10362/21941-
dc.descriptionThis study was supported by Fundacao para a Ciencia e Tecnologia (FCT) Grants PTDC/DTP-EPI/0207/2012 and PTDC/BIM-MET/0486/2012 and by the Portuguese Diabetes Society (SPD).-
dc.description.abstractNonalcoholic fatty liver disease (NAFLD) is rapidly becoming the most prevalent cause of liver disease worldwide and afflicts adults and children as currently associated with obesity and insulin resistance. Even though lately some advances have been made to elucidate the mechanism and causes of the disease much remains unknown about NAFLD. The aim of this paper is to discuss the present knowledge regarding the pathogenesis of the disease aiming at the initial steps ofNAFLD development, when inflammation impinges on fat liver deposition. At this stage, the Kupffer cells attain a prominent role. This knowledge becomes subsequently relevant for the development of future diagnostic, prevention, and therapeutic options for the management of NAFLD.en
dc.format.extent11-
dc.language.isoeng-
dc.relationinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/124913/PT-
dc.relationinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/124357/PT-
dc.rightsopenAccess-
dc.subjectRISK-FACTORS-
dc.subjectTOLL-LIKE RECEPTORS-
dc.subjectHEPATOCELLULAR-CARCINOMA-
dc.subjectFRUCTOSE-
dc.subjectFATTY LIVER-DISEASE-
dc.subjectINDUCED HEPATIC STEATOSIS-
dc.subjectINSULIN-RESISTANCE-
dc.subjectSTELLATE CELLS-
dc.subjectENDOPLASMIC-RETICULUM-
dc.subjectNONALCOHOLIC STEATOHEPATITIS-
dc.subjectFATTY LIVER-DISEASE-
dc.subjectTOLL-LIKE RECEPTORS-
dc.subjectINDUCED HEPATIC STEATOSIS-
dc.subjectINSULIN-RESISTANCE-
dc.subjectNONALCOHOLIC STEATOHEPATITIS-
dc.subjectHEPATOCELLULAR-CARCINOMA-
dc.subjectENDOPLASMIC-RETICULUM-
dc.subjectSTELLATE CELLS-
dc.subjectRISK-FACTORS-
dc.subjectFRUCTOSE-
dc.subjectSDG 3 - Good Health and Well-being-
dc.titleHow inflammation impinges on NAFLD: A role for Kupffer cells-
dc.typereview-
degois.publication.firstPage-
degois.publication.issueNA-
degois.publication.lastPage-
degois.publication.titleBioMed Research International-
degois.publication.volume984578-
dc.peerreviewedyes-
dc.identifier.doihttps://doi.org/10.1155/2015/984578-
dc.description.versionpublishersversion-
dc.description.versionpublished-
dc.contributor.institutionCentro de Estudos de Doenças Crónicas (CEDOC)-
dc.contributor.institutionNOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)-
Aparece nas colecções:NMS: CEDOC - Artigos em revista internacional com arbitragem científica

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