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ca2+/calmodulin-dependent kinase ii ca2+/calmodulin-dependent protein kinase tamoxifen-inducible mer/cre/mer expression ca2+/calmodulin kinase ii irreversible ischemia-reperfusion injury camp-dependent protein kinase tamoxifen-inducible cre protein inducible cardiomyocyte-specific deletion l-type calcium channels cardiac-specific nuclear delta month download article/chapter cam kinase ii calcineurin-dependent transcriptional pathway cardiac-specific αmhc promoter ca2+/calmodulin kinases camkii-dependent ventricular remodeling cardiac-specific gene transfer tissue-specific gene manipulations pro-inflammatory chemoattractant signaling cam kinase superfamily article basic research dependent camkii activation cardiac stress delays calcium-independent activation combined genetic deletion full article pdf overt heart failure combat heart failure related subjects pressure overload selectively pathological cardiac hypertrophy pathological cardiac genes s-nitrosylation induces differential cardiac remodeling induces dilated cardiomyopathy privacy choices/manage cookies nonfailing human hearts specific camkii inhibition myocardial cell apoptosis hermann-josef gröne structural heart disease cardiomyocyte hypertrophy german cardiac society nuclear factor-kappab �therapeutic” camkii deletion camkii inhibition protects heart failure heart failure article kreusser original contribution

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         headline:Inducible cardiomyocyte-specific deletion of CaM kinase II protects from pressure overload-induced heart failure
         description:CaM kinase II (CaMKII) has been suggested to drive pathological cardiac remodeling and heart failure. However, the evidence provided so far is based on inhibitory strategies using chemical compounds and peptides that also exert off-target effects and followed exclusively preventive strategies. Therefore, the aim of this study was to investigate whether specific CaMKII inhibition after the onset of cardiac stress delays or reverses maladaptive cardiac remodeling and dysfunction. Combined genetic deletion of the two redundant CaMKII genes δ and γ was induced after the onset of overt heart failure as the result of pathological pressure overload induced by transverse aortic constriction (TAC). We used two different strategies to engineer an inducible cardiomyocyte-specific CaMKIIδ/CaMKIIγ double knockout mouse model (DKO): one model bases on tamoxifen-inducible mER/Cre/mER expression under control of the cardiac-specific αMHC promoter; the other strategy bases on overexpression of Cre recombinase via cardiac-specific gene transfer through adeno-associated virus (AAV9) under control of the cardiac-specific myosin light chain promoter. Both models led to a substantial deletion of CaMKII in failing hearts. To approximate the clinical situation, CaMKII deletion was induced 3 weeks after TAC surgery. In both models of DKO, the progression of cardiac dysfunction and interstitial fibrosis could be slowed down as compared to control animals. Taken together, we show for the first time that “therapeutic” CaMKII deletion after cardiac damage is sufficient to attenuate maladaptive cardiac remodeling and to reverse signs of heart failure. These data suggest that CaMKII inhibition is a promising therapeutic approach to combat heart failure.
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      headline:Inducible cardiomyocyte-specific deletion of CaM kinase II protects from pressure overload-induced heart failure
      description:CaM kinase II (CaMKII) has been suggested to drive pathological cardiac remodeling and heart failure. However, the evidence provided so far is based on inhibitory strategies using chemical compounds and peptides that also exert off-target effects and followed exclusively preventive strategies. Therefore, the aim of this study was to investigate whether specific CaMKII inhibition after the onset of cardiac stress delays or reverses maladaptive cardiac remodeling and dysfunction. Combined genetic deletion of the two redundant CaMKII genes δ and γ was induced after the onset of overt heart failure as the result of pathological pressure overload induced by transverse aortic constriction (TAC). We used two different strategies to engineer an inducible cardiomyocyte-specific CaMKIIδ/CaMKIIγ double knockout mouse model (DKO): one model bases on tamoxifen-inducible mER/Cre/mER expression under control of the cardiac-specific αMHC promoter; the other strategy bases on overexpression of Cre recombinase via cardiac-specific gene transfer through adeno-associated virus (AAV9) under control of the cardiac-specific myosin light chain promoter. Both models led to a substantial deletion of CaMKII in failing hearts. To approximate the clinical situation, CaMKII deletion was induced 3 weeks after TAC surgery. In both models of DKO, the progression of cardiac dysfunction and interstitial fibrosis could be slowed down as compared to control animals. Taken together, we show for the first time that “therapeutic” CaMKII deletion after cardiac damage is sufficient to attenuate maladaptive cardiac remodeling and to reverse signs of heart failure. These data suggest that CaMKII inhibition is a promising therapeutic approach to combat heart failure.
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Analytics and Tracking {📊}

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Libraries {📚}

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CDN Services {📦}

• Crossref