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http://purl.uniprot.org/citations/31285482http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31285482http://www.w3.org/2000/01/rdf-schema#comment"Calcium/calmodulin-dependent protein kinase type II delta (CaMKIIδ), the predominant CaMKII isoform expressed in the heart, has been implicated in the progression of myocardial infarction- and pressure overload-induced pathological remodeling. However, the role of CaMKIIδ in volume overload (VO) has not been explored. We have previously reported an activation of CaMKII during transition to HF in long-term VO. Here, we address whether CaMKIIδ is critically involved in the mortality, myocardial remodeling, and heart failure (HF) progression in response to VO. CaMKIIδ knockout (δ-KO) and wild-type (WT) littermates were exposed to aortocaval shunt-induced VO, and the progression of adverse myocardial remodeling was assessed by serial echocardiography, histological and molecular analyses. The mortality rates during 10 weeks of VO were similar in δ-KO and WT mice. Both genotypes displayed comparable eccentric myocardial hypertrophy, altered left ventricle geometry, perturbed systolic and diastolic functions after shunt. Additionally, cardiomyocytes hypertrophy, augmented myocyte apoptosis, and up-regulation of hypertrophic genes were also not significantly different in δ-KO versus WT hearts after shunt. Therefore, CaMKIIδ signaling seems to be dispensable for the progression of VO-induced maladaptive cardiac remodeling. Accordingly, we hypothesize that CaMKIIδ-inhibition as a therapeutic approach might not be helpful in the context of VO-triggered HF."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.org/dc/terms/identifier"doi:10.1038/s41598-019-46332-3"xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/author"Hasenfuss G."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/author"Mohamed B.A."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/author"Toischer K."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/author"Schnelle M."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/author"Elkenani M."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/author"Jakubiczka-Smorag J."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/author"Buchholz E."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/author"Koszewa S."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/author"Lbik D."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/name"Sci Rep"xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/pages"9889"xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/title"Genetic deletion of calcium/calmodulin-dependent protein kinase type II delta does not mitigate adverse myocardial remodeling in volume-overloaded hearts."xsd:string
http://purl.uniprot.org/citations/31285482http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/31285482http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31285482
http://purl.uniprot.org/citations/31285482http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31285482
http://purl.uniprot.org/uniprot/#_A0A0G2JGS4-mappedCitation-31285482http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31285482
http://purl.uniprot.org/uniprot/#_E9QAJ4-mappedCitation-31285482http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31285482
http://purl.uniprot.org/uniprot/#_E9Q1T1-mappedCitation-31285482http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31285482
http://purl.uniprot.org/uniprot/#_E9Q1V9-mappedCitation-31285482http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31285482
http://purl.uniprot.org/uniprot/#_E9Q1W0-mappedCitation-31285482http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31285482
http://purl.uniprot.org/uniprot/#_D6RDQ8-mappedCitation-31285482http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31285482