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Calcium/calmodulin-dependent protein kinase II couples wnt signaling with histone deacetylase 4 and mediates dishevelled-induced cardiomyopathy

Activation of Wnt signaling results in maladaptive cardiac remodeling and cardiomyopathy. Recently, calcium/calmodulin-dependent protein kinase II (CaMKII) was reported to be a pivotal participant in myocardial remodeling. Because CaMKII was suggested as a downstream target of noncanonical Wnt signa...

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Bibliographische Detailangaben
Hauptverfasser: Zhang, Min (VerfasserIn) , Riffel, Johannes (VerfasserIn) , Kreußer, Michael (VerfasserIn) , Katus, Hugo (VerfasserIn) , Backs, Johannes (VerfasserIn) , Hardt, Stefan (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 2015
In: Hypertension
Year: 2015, Jahrgang: 65, Heft: 2, Pages: 335-344
ISSN:1524-4563
DOI:10.1161/HYPERTENSIONAHA.114.04467
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1161/HYPERTENSIONAHA.114.04467
Verlag, lizenzpflichtig, Volltext: https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.114.04467
Volltext
Verfasserangaben:Zhang Min, Hagenmueller Marco, Riffel Johannes H., Kreusser Michael M., Bernhold Elmar, Fan Jingjing, Katus Hugo A., Backs Johannes, and Hardt Stefan E.
Beschreibung
Zusammenfassung:Activation of Wnt signaling results in maladaptive cardiac remodeling and cardiomyopathy. Recently, calcium/calmodulin-dependent protein kinase II (CaMKII) was reported to be a pivotal participant in myocardial remodeling. Because CaMKII was suggested as a downstream target of noncanonical Wnt signaling, we aimed to elucidate the role of CaMKII in dishevelled-1-induced cardiomyopathy and the mechanisms underlying its function. Dishevelled-1-induced cardiomyopathy was reversed by deletion of neither CaMKIIδ nor CaMKIIγ. Therefore, dishevelled-1-transgenic mice were crossed with CaMKIIδγ double-knockout mice. These mice displayed a normal cardiac phenotype without cardiac hypertrophy, fibrosis, apoptosis, or left ventricular dysfunction. Further mechanistic analyses unveiled that CaMKIIδγ couples noncanonical Wnt signaling to histone deacetylase 4 and myosin enhancer factor 2. Therefore, our findings indicate that the axis, consisting of dishevelled-1, CaMKII, histone deacetylase 4, and myosin enhancer factor 2, is an attractive therapeutic target for prevention of cardiac remodeling and its progression to left ventricular dysfunction.
Beschreibung:Gesehen am 28.07.2020
Originally published 8 Dec 2014
Beschreibung:Online Resource
ISSN:1524-4563
DOI:10.1161/HYPERTENSIONAHA.114.04467

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