ArticleHeart rhythm2013
Inhibition of CaMKII phosphorylation of RyR2 prevents inducible ventricular arrhythmias in mice with Duchenne muscular dystrophy.
Article in Heart rhythm, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 48 citations in OpenAlex.
- Cyclic AMP-dependent regulation of ryanodine receptors in healthy and diseased hearts.Journal of molecular and cellular cardiology · 2026Review
- Deletion of Exon 51 in a Humanized Duchenne Muscular Dystrophy Mouse Model Abolishes Ventricular Arrhythmia Predisposition.Circulation. Genomic and precision medicine · 2025Article
- S-nitrosylation of cardiac myocyte proteins may underlie sex differences in cardiac disease.Frontiers in physiology · 2025Review
- Right ventricular preload and afterload challenge induces contractile dysfunction and arrhythmia in isolated hearts of dystrophin-deficient male mice.Physiological reports · 2024Article
- Efficacy of exon-skipping therapy for DMD cardiomyopathy with mutations in actin binding domain 1.Molecular therapy. Nucleic acids · 2023Article
- Calcium handling dysfunction and cardiac damage following acute ventricular preload challenge in the dystrophin-deficient mouse heart.American journal of physiology. Heart and circulatory physiology · 2023Article
- Cryo-EM analysis of scorpion toxin binding to Ryanodine Receptors reveals subconductance that is abolished by PKA phosphorylation.Science advances · 2023Article
- Genome Editing and Cardiac Arrhythmias.Cells · 2023Review
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype.EMBO molecular medicine · 2022Article
- Calcium handling maturation and adaptation to increased substrate stiffness in human iPSC-derived cardiomyocytes: The impact of full-length dystrophin deficiency.Frontiers in physiology · 2022Article
- Chai-Hu-San-Shen Capsule Ameliorates Ventricular Arrhythmia Through Inhibition of the CaMKII/FKBP12.6/RyR2/CaEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Pathological conformations of disease mutant Ryanodine Receptors revealed by cryo-EM.Nature communications · 2021Article
- CaMKII Inhibition is a Novel Therapeutic Strategy to Prevent Diabetic Cardiomyopathy.Frontiers in pharmacology · 2021Review
- Multisite phosphorylation of the cardiac ryanodine receptor: a random or coordinated event?Pflugers Archiv : European journal of physiology · 2020Review
- Genetic basis and molecular biology of cardiac arrhythmias in cardiomyopathies.Cardiovascular research · 2020Review
- Prevention of connexin-43 remodeling protects against Duchenne muscular dystrophy cardiomyopathy.The Journal of clinical investigation · 2020Article
- Regulation of Mitochondrial ATP Production: CaTrends in molecular medicine · 2020Review
- S-nitrosylation of connexin43 hemichannels elicits cardiac stress-induced arrhythmias in Duchenne muscular dystrophy mice.JCI insight · 2019Article
- Metabolic Alterations in Cardiomyocytes of Patients with Duchenne and Becker Muscular Dystrophies.Journal of clinical medicine · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundVentricular tachycardia (VT) is the second most common cause of death in patients with Duchenne muscular dystrophy (DMD). Recent studies have implicated enhanced sarcoplasmic reticulum (SR) Ca(2+) leak via type 2 ryanodine receptor (RyR2) as a cause of VT in the mdx mouse model of DMD. However, the signaling mechanisms underlying induction of SR Ca(2+) leak and VT are poorly understood.
objectiveTo test whether enhanced Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphorylation of RyR2 underlies SR Ca(2+) leak and induction of VT in mdx mice.
methodsProgrammed electrical stimulation was performed on anesthetized mice and confocal imaging of Ca(2+) release events in isolated ventricular myocytes.
resultsProgrammed electrical stimulation revealed inducible VT in mdx mice, which was inhibited by CaMKII inhibition or mutation S2814A in RyR2. Myocytes from mdx mice exhibited more Ca(2+) sparks and Ca(2+) waves compared with wild-type mice, in particular at faster pacing rates. Arrhythmogenic Ca(2+) waves were inhibited by CaMKII but not by protein kinase A inhibition. Moreover, mutation S2814A but not S2808A in RyR2 suppressed spontaneous Ca(2+) waves in myocytes from mdx mice.
conclusionsCaMKII blockade and genetic inhibition of RyR2-S2814 phosphorylation prevent VT induction in a mouse model of DMD. In ventricular myocytes from mdx mice, spontaneous Ca(2+) sparks and Ca(2+) waves can be suppressed by CaMKII inhibition or mutation S2814A in RyR2. Thus, the inhibition of CaMKII-induced SR Ca(2+) leak might be a new strategy to prevent arrhythmias in patients with DMD without heart failure.
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