ArticleJournal of molecular and cellular cardiology2011
Calcium-calmodulin dependent protein kinase II (CaMKII): a main signal responsible for early reperfusion arrhythmias.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 94 citations in OpenAlex.
- Exercise preconditioning reduces the electrostimulation-induced incidence of arrhythmias in exhausted rats by regulating the CaMKⅡ-RyR2 signaling pathway.Journal of cardiothoracic surgery · 2026Article
- Sepsis-Induced Cardiomyopathy and Cardiac Arrhythmias: Pathophysiology and Implications for Novel Therapeutic Approaches.Biomedicines · 2025Review
- Electrocardiographic Changes in Patients With Hypokalemia and Their Correlation With Serum Potassium Levels.Cureus · 2025Article
- The Dysfunction of CaInternational journal of molecular sciences · 2023Review
- Pharmacological Modulation by Low Molecular Weight Heparin of Purinergic Signaling in Cardiac Cells Prevents Arrhythmia and Lethality Induced by Myocardial Infarction.Journal of cardiovascular development and disease · 2023Article
- Myocardial oxidative stress is increased in early reperfusion, but systemic antioxidative therapy does not prevent ischemia-reperfusion arrhythmias in pigs.Frontiers in cardiovascular medicine · 2023Article
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- Therapeutic Approaches of Ryanodine Receptor-Associated Heart Diseases.International journal of molecular sciences · 2022Review
- Chai-Hu-San-Shen Capsule Ameliorates Ventricular Arrhythmia Through Inhibition of the CaMKII/FKBP12.6/RyR2/CaEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Uridine treatment prevents myocardial injury in rat models of acute ischemia and ischemia/reperfusion by activating the mitochondrial ATP-dependent potassium channel.Scientific reports · 2021Article
- mTOR-mediated calcium transients affect cardiac function in ex vivo ischemia-reperfusion injury.Physiological reports · 2021Article
- Mechanisms underlying pathological CaPflugers Archiv : European journal of physiology · 2021Review
- Elevated perfusate [NaScientific reports · 2020Article
- Cardiac arrhythmias in patients with COVID-19.Journal of arrhythmia · 2020Review
- Genetic Loss ofCirculation. Arrhythmia and electrophysiology · 2020Article
- Tilianin Protects against Ischemia/Reperfusion-Induced Myocardial Injury through the Inhibition of the CaBioMed research international · 2020Article
- The Role of Cardiac Macrophage and Cytokines on Ventricular Arrhythmias.Frontiers in physiology · 2020Review
- Review
- Ablation of phospholamban rescues reperfusion arrhythmias but exacerbates myocardium infarction in hearts with Ca2+/calmodulin kinase II constitutive phosphorylation of ryanodine receptors.Cardiovascular research · 2019Article
- Inhibitor 1 of Protein Phosphatase 1 Regulates CaOxidative medicine and cellular longevity · 2019Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
To explore whether CaMKII-dependent phosphorylation events mediate reperfusion arrhythmias, Langendorff perfused hearts were submitted to global ischemia/reperfusion. Epicardial monophasic or transmembrane action potentials and contractility were recorded. In rat hearts, reperfusion significantly increased the number of premature beats (PBs) relative to pre-ischemic values. This arrhythmic pattern was associated with a significant increase in CaMKII-dependent phosphorylation of Ser2814 on Ca(2+)-release channels (RyR2) and Thr17 on phospholamban (PLN) at the sarcoplasmic reticulum (SR). These phenomena could be prevented by the CaMKII-inhibitor KN-93. In transgenic mice with targeted inhibition of CaMKII at the SR membranes (SR-AIP), PBs were significantly decreased from 31±6 to 5±1 beats/3min with a virtually complete disappearance of early-afterdepolarizations (EADs). In mice with genetic mutation of the CaMKII phosphorylation site on RyR2 (RyR2-S2814A), PBs decreased by 51.0±14.7%. In contrast, the number of PBs upon reperfusion did not change in transgenic mice with ablation of both PLN phosphorylation sites (PLN-DM). The experiments in SR-AIP mice, in which the CaMKII inhibitor peptide is anchored in the SR membrane but also inhibits CaMKII regulation of L-type Ca(2+) channels, indicated a critical role of CaMKII-dependent phosphorylation of SR proteins and/or L-type Ca(2+) channels in reperfusion arrhythmias. The experiments in RyR2-S2814A further indicate that up to 60% of PBs related to CaMKII are dependent on the phosphorylation of RyR2-Ser2814 site and could be ascribed to delayed-afterdepolarizations (DADs). Moreover, phosphorylation of PLN-Thr17 and L-type Ca(2+) channels might contribute to reperfusion-induced PBs, by increasing SR Ca(2+) content and Ca(2+) influx.
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