http://purl.uniprot.org/citations/17210832 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/17210832 | http://www.w3.org/2000/01/rdf-schema#comment | "The hypertrophic response of the heart has been recognized recently as the net result of activation of prohypertrophic and antihypertrophic pathways. Here we report the involvement of the Wnt/Frizzled pathway in the onset of cardiac hypertrophy development. Stimulation of the Wnt/Frizzled pathway activates the disheveled (Dvl) protein. Disheveled subsequently can inhibit glycogen synthase kinase-3beta, a protein with potent antihypertrophic actions through diverse molecular mechanisms. In the Wnt/Frizzled pathway, inhibition of glycogen synthase kinase-3beta leads to an increased amount of beta-catenin, which can act as a transcription factor for several hypertrophy-associated target genes. In this study we subjected mice lacking the Dvl-1 gene and their wild-type littermates to thoracic aortic constriction for 7, 14, and 35 days. In mice lacking the Dvl-1 gene, 7 days of pressure overload-induced increases in left ventricular posterior wall thickness and expression of atrial natriuretic factor and brain natriuretic protein were attenuated compared with their wild-type littermates. Beta-catenin protein amount was reduced in the group lacking the Dvl-1 gene, and an increased glycogen synthase kinase-3beta activity was observed. Moreover, the increase in the amount of Ser(473)-phosphorylated Akt, a stimulator of cardiac hypertrophy, was lower in the group lacking the Dvl-1 gene. In conclusion, we have demonstrated that interruption of Wnt signaling in the mice lacking the Dvl-1 gene attenuates the onset of pressure overload-induced cardiac hypertrophy through mechanisms involving glycogen synthase kinase-3beta and Akt. Therefore, the Wnt/Frizzled pathway may provide novel therapeutic targets for antihypertrophic therapy."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.org/dc/terms/identifier | "doi:10.1161/01.hyp.0000255946.55091.24"xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/author | "Wynshaw-Boris A."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/author | "Janssen B.J."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/author | "Blankesteijn W.M."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/author | "Smits J.F."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/author | "Langen R.C."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/author | "van der Velden J.L."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/author | "Strzelecka A.E."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/author | "van de Schans V.A."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/author | "van den Borne S.W."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/name | "Hypertension"xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/pages | "473-480"xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/title | "Interruption of Wnt signaling attenuates the onset of pressure overload-induced cardiac hypertrophy."xsd:string |
http://purl.uniprot.org/citations/17210832 | http://purl.uniprot.org/core/volume | "49"xsd:string |
http://purl.uniprot.org/citations/17210832 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17210832 |
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