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...
Gespeichert in:
| Hauptverfasser: | , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2015
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| 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 
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| Verfasserangaben: | Zhang Min, Hagenmueller Marco, Riffel Johannes H., Kreusser Michael M., Bernhold Elmar, Fan Jingjing, Katus Hugo A., Backs Johannes, and Hardt Stefan E. |
MARC
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| 245 | 1 | 0 | |a Calcium/calmodulin-dependent protein kinase II couples wnt signaling with histone deacetylase 4 and mediates dishevelled-induced cardiomyopathy |c Zhang Min, Hagenmueller Marco, Riffel Johannes H., Kreusser Michael M., Bernhold Elmar, Fan Jingjing, Katus Hugo A., Backs Johannes, and Hardt Stefan E. |
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| 520 | |a 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. | ||
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