ArticleHeart rhythm2019
Calcium/calmodulin-dependent protein kinase II causes atrial structural remodeling associated with atrial fibrillation and heart failure.
Article in Heart rhythm, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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
38 citing papers in PubMed, 53 citations in OpenAlex.
- Hederagenin Attenuates Morphine Addiction via GABAA1-Mediated Modulation of CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Computational modeling identifies protective mechanisms of estrogen and testosterone against atrial fibrosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Cellular Senescence and the SASP in HFpEF: Pathogenic Mechanisms and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- [Integrating Bioinformatics and Machine Learning Algorithms to Screen Inflammatory Biomarkers for Atrial Fibrillation and Experimental Validation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Article
- BET inhibitors in cardiovascular diseases: from atherosclerosis to heart failure.Pharmacological reports : PR · 2026Review
- Mechanisms of Atrial Fibrillation in Heart Failure: Uncovering Therapeutic Targets in the Atrial Substrate.Current heart failure reports · 2026Review
- Oxidative Stress, Mitochondrial Homeostasis, and Sirtuins in Atrial Fibrillation.International journal of molecular sciences · 2025Review
- Gene Therapies in Atrial Fibrillation.Journal of cardiovascular translational research · 2025Review
- Recent Advances in Inflammation-Associated Epicardial Adipose Tissue for Atrial Fibrillation Patients.Reviews in cardiovascular medicine · 2025Review
- Computational modelling of cardiac fibroblast signalling reveals a key role for CaThe Journal of physiology · 2025Article
- Systemic immune inflammation index as a predictor for atrial fibrillation recurrence after catheter ablation.World journal of cardiology · 2025Article
- Association between ALDH2 rs671 polymorphism and susceptibility to non-valvular atrial fibrillation in a Chinese population: a large-scale case-control study.Frontiers in physiology · 2025Article
- Secretoneurin plasma levels are decreased after catheter ablation for atrial fibrillation-patients with AF produce lower SN levels than healthy individuals: the SAFE registry.Frontiers in cardiovascular medicine · 2025Article
- Gene therapy for atrial fibrillation.Journal of molecular and cellular cardiology · 2024Review
- Oxidative stress and atrial fibrillation.Journal of molecular and cellular cardiology · 2024Review
- Molecular remodeling in comorbidities associated with heart failure: a current update.Molecular biology reports · 2024Review
- Atrial fibrillation in cancer, anticancer therapies, and underlying mechanisms.Journal of molecular and cellular cardiology · 2024Review
- Empagliflozin inhibits increased Na influx in atrial cardiomyocytes of patients with HFpEF.Cardiovascular research · 2024Article
- A structure-based computational model of IPBiophysical journal · 2024Article
- Increased Risk for Atrial Alternans in Rabbit Heart Failure: The Role of CaBiomolecules · 2023Article
Corrections and comments
- Commented on byAtrial Ca2019
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundAtrial fibrillation (AF) is sustained by reentrant mechanisms that depend, in part, on atrial structural remodeling. Increased Ca
objectiveThe purpose of this study was to assess the effects of CaMKII on AF-related structural remodeling.
methodsWe evaluated the objective in a porcine AF-heart failure model using atrial gene transfer of the CaMKII inhibitory peptide CaMKIIn. We used conventional methods including in vivo electrophysiological study, telemetry, western blot, echocardiography, and histology to quantify rhythm, function, microstructure, and signaling pathways relevant to CaMKII and structural remodeling.
resultsCaMKII levels and activity increased progressively in the early stages of AF-heart failure. Inhibiting CaMKII preserved atrial contractile function and attenuated atrial hypertrophy, fibrosis, and apoptosis but did not affect inflammation or myolysis. These effects were accompanied by significantly decreased phosphorylation of HDAC4, decreased expression of p38MAP-kinase, and alterations in the phosphorylation pattern and relative ratios of JNK isoforms.
conclusionOur findings suggest that CaMKII mediates signaling pathways related to atrial contractile function and structural remodeling in AF. CaMKII inhibition is potentially a novel therapy for AF. These findings are of importance because no clinically relevant mediators of either atrial contractile function or structural remodeling have yet been identified.
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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.