| http://purl.uniprot.org/citations/28785686 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28785686 | http://www.w3.org/2000/01/rdf-schema#comment | "AimsHypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy, diastolic dysfunction and increased interstitial fibrosis. Current treatment is based on beta-adrenoceptor (AR) and calcium channel blockers. Since mice deficient of protein phosphatase-1 inhibitor-1 (I-1), an amplifier in beta-AR signalling, were protected from pathological adrenergic stimulation in vivo, we hypothesized that I-1 ablation could result in an improved outcome in a HCM mouse model.Methods and resultsWe crossed mice deficient of I-1 with homozygous myosin-binding protein C knock-out (Mybpc3 KO) mice exhibiting cardiac dilatation and reduced survival. Unexpectedly, survival time was shorter in double I-1/Mybpc3 KO than in single Mybpc3 KO mice. Longitudinal echocardiographic assessment revealed lower fractional area change, and higher diastolic left ventricular inner dimensions and end-diastolic volumes in Mybpc3 KO than in WT mice. In comparison to Mybpc3 KO, double I-1/Mybpc3 KO presented higher left ventricular end-diastolic volumes, inner dimensions and ventricular surface areas with increasing differences over time. Phosphorylation levels of PKA-downstream targets and mRNA levels of hypertrophic markers did not differ between I-1/Mybpc3 KO and single Mybpc3 KO mice, except a trend towards higher beta-myosin heavy chain levels in double I-1/Mybpc3 KO.ConclusionThe data indicate that interference with beta-AR signalling has no long-term benefit in this severe MYBPC3-related cardiomyopathy mouse model."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ijcha.2015.05.010"xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/author | "Weber S."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/author | "Carrier L."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/author | "Eschenhagen T."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/author | "Friedrich F.W."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/author | "Reischmann S."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/author | "El-Armouche A."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/author | "Geertz B."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/author | "Flenner F."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/author | "Sotoud H."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/name | "Int J Cardiol Heart Vasc"xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/pages | "87-94"xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/title | "I-1-deficiency negatively impacts survival in a cardiomyopathy mouse model."xsd:string |
| http://purl.uniprot.org/citations/28785686 | http://purl.uniprot.org/core/volume | "8"xsd:string |
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