ArticleBasic research in cardiology2016
Inducible cardiomyocyte-specific deletion of CaM kinase II protects from pressure overload-induced heart failure.
Article in Basic research in cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
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- PP2A-B56α is a key determinant of cardiac protein phosphorylation and functional responses to β-adrenergic signalling.Journal of molecular and cellular cardiology plus · 2025Article
- PRMT1 alleviates isoprenaline-induced myocardial hypertrophy by methylating SRSF1.Acta biochimica et biophysica Sinica · 2024Article
- Preparation of Nanoparticles Loaded with Membrane-Impermeable Peptide AC3-I and Its Protective Effect on Myocardial Ischemia and Reperfusion.Pharmaceutics · 2024Article
- Role of CAMK2D in neurodevelopment and associated conditions.American journal of human genetics · 2024Article
- Inhibition of bromodomain extraterminal histone readers alleviates skin fibrosis in experimental models of scleroderma.JCI insight · 2022Article
- Splicing and Dicing: A Deeper Dive Into CaMKIIδ and Cardiac Inflammation.Circulation research · 2022Article
- Emerging therapeutic targets for cardiac hypertrophy.Expert opinion on therapeutic targets · 2022Review
- Calcium Regulation on the Atrial Regional Difference of Collagen Production Activity in Atrial Fibrogenesis.Biomedicines · 2021Article
- Chronic CaThe Journal of pharmacology and experimental therapeutics · 2021Article
- 4-hydroxytamoxifen does not deteriorate cardiac function in cardiomyocyte-specific MerCreMer transgenic mice.Basic research in cardiology · 2021Article
- Vascular endothelial growth factor enhances profibrotic activities through modulation of calcium homeostasis in human atrial fibroblasts.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Evaluation of the Effects ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Huoxue Wentong Formula ameliorates myocardial infarction in rats through inhibiting CaMKII oxidation and phosphorylation.Chinese medicine · 2020Article
- Inflammation in nonischemic heart disease: initiation by cardiomyocyte CaMKII and NLRP3 inflammasome signaling.American journal of physiology. Heart and circulatory physiology · 2019Review
- All-trans retinoic acid attenuates isoproterenol-induced cardiac dysfunction through Crabp1 to dampen CaMKII activation.European journal of pharmacology · 2019Article
- CaMKII activation participates in doxorubicin cardiotoxicity and is attenuated by moderate GRP78 overexpression.PloS one · 2019Article
- Cardiac CaMKII activation promotes rapid translocation to its extra-dyadic targets.Journal of molecular and cellular cardiology · 2018Article
- Physiological and unappreciated roles of CaMKII in the heart.Basic research in cardiology · 2018Review
- Inhibition of calcium/calmodulin-dependent kinase II restores contraction and relaxation in isolated cardiac muscle from type 2 diabetic rats.Cardiovascular diabetology · 2018Article
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9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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