ReviewFrontiers in pharmacology2014
Calcium dysregulation in atrial fibrillation: the role of CaMKII.
Review in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 71 citations in OpenAlex.
- Exploring the role of CaMKII in exercise-induced cardioprotection.Human cell · 2026Review
- Frataxin deficiency drives cardiac dysfunction and transcriptional dysregulation in Friedreich ataxia iPSC model.Cell death & disease · 2026Article
- Associations of the triglyceride-glucose index and its obesity-related derivatives with cardiac structure, function, and incident atrial fibrillation: a prospective cohort study using cardiac magnetic resonance.Cardiovascular diabetology · 2026Article
- Atrial Cardiomyopathy and Atrial Fibrillation in Different Heart Failure Substrates.Arrhythmia & electrophysiology review · 2026Review
- Autonomic dysregulation and atrial arrhythmias.American journal of physiology. Cell physiology · 2025Review
- Computational modelling of cardiac fibroblast signalling reveals a key role for CaThe Journal of physiology · 2025Article
- Nicotine Exacerbates Arrhythmogenesis in Rabbit Right Ventricular Outflow Tract Triggered by Chronic Obstructive Pulmonary Disease.Journal of cellular and molecular medicine · 2025Article
- KFrontiers in physiology · 2025Article
- Gene therapy for atrial fibrillation.Journal of molecular and cellular cardiology · 2024Review
- Atrial fibrillation in cancer, anticancer therapies, and underlying mechanisms.Journal of molecular and cellular cardiology · 2024Review
- Clonal Hematopoiesis of Indeterminate Potential With Loss ofCirculation · 2024Article
- Integrative human atrial modelling unravels interactive protein kinase A and Ca2+/calmodulin-dependent protein kinase II signalling as key determinants of atrial arrhythmogenesis.Cardiovascular research · 2023Article
- Loss of the Atrial Fibrillation-Related Gene,Circulation research · 2023Article
- Timing mechanisms to control heart rhythm and initiate arrhythmias: roles for intracellular organelles, signalling pathways and subsarcolemmal CaPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Mouse models of spontaneous atrial fibrillation.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- Electrophysiological and calcium-handling development during long-term culture of human-induced pluripotent stem cell-derived cardiomyocytes.Basic research in cardiology · 2023Article
- Inhibition of EPAC1 signaling pathway alters atrial electrophysiology and prevents atrial fibrillation.Frontiers in physiology · 2023Article
- ROCK (RhoA/Rho Kinase) Activation in Atrial Fibrillation: Molecular Pathways and Clinical Implications.Current cardiology reviews · 2023Article
- Screening of atrial fibrillation diagnostic markers based on a GEO database chip and bioinformatics analysis.Journal of thoracic disease · 2022Article
- Mirabegron, a β3‑adrenoreceptor agonist, regulates right and left atrial arrhythmogenesis differently.Experimental and therapeutic medicine · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Atrial fibrillation (AF) is the most frequently encountered clinical arrhythmia and is associated with increased morbidity and mortality. Ectopic activity and reentry are considered major arrhythmogenic mechanisms contributing to the initiation and maintenance of AF. In addition, AF is self-reinforcing through progressive electrical and structural remodeling which stabilize the arrhythmia and make it more difficult to treat. Recent research has suggested an important role for Ca(2+)-dysregulation in AF. Ca(2+)-handling abnormalities may promote ectopic activity, conduction abnormalities facilitating reentry, and AF-related remodeling. In this review article, we summarize the Ca(2+)-handling derangements occurring in AF and discuss their impact on fundamental arrhythmogenic mechanisms. We focus in particular on the role of the multifunctional Ca(2+)/calmodulin-dependent protein kinase type-II (CaMKII), which acts as a major link between Ca(2+)-dysregulation and arrhythmogenesis. CaMKII expression and activity are increased in AF and promote arrhythmogenesis through phosphorylation of various targets involved in cardiac electrophysiology and excitation-contraction coupling. We discuss the implications for potential novel therapeutic strategies for AF based on CaMKII and Ca(2+)-handling abnormalities.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.