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http://purl.uniprot.org/citations/17210832http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17210832http://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/17210832http://purl.org/dc/terms/identifier"doi:10.1161/01.hyp.0000255946.55091.24"xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/author"Wynshaw-Boris A."xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/author"Janssen B.J."xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/author"Blankesteijn W.M."xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/author"Smits J.F."xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/author"Langen R.C."xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/author"van der Velden J.L."xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/author"Strzelecka A.E."xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/author"van de Schans V.A."xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/author"van den Borne S.W."xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/name"Hypertension"xsd:string
http://purl.uniprot.org/citations/17210832http://purl.uniprot.org/core/pages"473-480"xsd:string
http://purl.uniprot.org/citations/17210832http://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/17210832http://purl.uniprot.org/core/volume"49"xsd:string
http://purl.uniprot.org/citations/17210832http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17210832
http://purl.uniprot.org/citations/17210832http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17210832
http://purl.uniprot.org/uniprot/#_P51141-mappedCitation-17210832http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17210832
http://purl.uniprot.org/uniprot/#_P31750-mappedCitation-17210832http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17210832
http://purl.uniprot.org/uniprot/#_Q3TRW4-mappedCitation-17210832http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17210832
http://purl.uniprot.org/uniprot/#_Q571M1-mappedCitation-17210832http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17210832
http://purl.uniprot.org/uniprot/Q3TRW4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17210832
http://purl.uniprot.org/uniprot/P51141http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17210832