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dc.contributor.authorAbraityte, Aurelija
dc.contributor.authorLunde, Ida Gjervold
dc.contributor.authorAskevold, Erik Tandberg
dc.contributor.authorMichelsen, Annika E.
dc.contributor.authorChristensen, Geir Arve
dc.contributor.authorAukrust, Pål
dc.contributor.authorYndestad, Arne
dc.contributor.authorFiane, Arnt
dc.contributor.authorAndreassen, Arne
dc.contributor.authorAakhus, Svend
dc.contributor.authorDahl, Christen Peder
dc.contributor.authorGullestad, Lars
dc.contributor.authorBroch, Kaspar
dc.contributor.authorUeland, Thor
dc.date.accessioned2018-03-01T09:23:06Z
dc.date.available2018-03-01T09:23:06Z
dc.date.issued2017-06-14
dc.description.abstractThe Wingless (Wnt) pathway has been implicated in the pathogenesis of dilated cardiomyopathy (DCM). To explore the role of Wnt modulators Wnt5a and sFRP3 in DCM patients we analyzed the expression of Wnt5a and sFRP3 in plasma and myocardium of DCM patients and evaluated their effects on NFAT luciferase activity in neonatal mouse cardiomyocytes. Elevated circulating Wnt5a (n = 102) was associated with increased pulmonary artery pressures, decreased right ventricular function and adverse outcome, with a stronger association in more severely affected patients. A higher Wnt5a/sFRP3 ratio (n = 25) was found in the right ventricle vs. the left ventricle and was correlated with NFAT activation as well as pulmonary artery pressures. Wnt5a induced NFAT activation and sFRP3 release in cardiomyocytes in vitro, while sFRP3 antagonized Wnt5a. Wnt5a is associated with right ventricular dysfunction and adverse outcome in DCM patients and may promote the progression of DCM through NFAT signaling.en_US
dc.descriptionSource at <a href=https://doi.org/10.1038/s41598-017-03625-9> https://doi.org/10.1038/s41598-017-03625-9 </a>.en_US
dc.identifier.citationAbraityte, JA., Lunde, I.G., Askevold, E.T., Michelsen, A.E., Christensen, G.A., Aukrust, P. ... Ueland, T. (2017). Wnt5a is associated with right ventricular dysfunction and adverse outcome in dilated cardiomyopathy. Scientific Reports. 7:3490en_US
dc.identifier.cristinIDFRIDAID 1494044
dc.identifier.doi10.1038/s41598-017-03625-9
dc.identifier.issn2045-2322
dc.identifier.urihttps://hdl.handle.net/10037/12233
dc.language.isoengen_US
dc.publisherNature Publishing Groupen_US
dc.relation.journalScientific Reports
dc.relation.projectIDinfo:eu-repo/grantAgreement/RCN/FRIMEDBIO/239950/Norway/Proteoglycan Signaling Induces Myocardial Fibrosis and Diastolic Heart Failure//en_US
dc.relation.projectIDThe Simon Fougner Hartmanns Family Foundationen_US
dc.rights.accessRightsopenAccessen_US
dc.subjectCardiomyopathiesen_US
dc.subjectCardiac hypertrophyen_US
dc.subjectVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Kardiologi: 771en_US
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Cardiology: 771en_US
dc.titleWnt5a is associated with right ventricular dysfunction and adverse outcome in dilated cardiomyopathyen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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