ArticleJCI insight2018
CaMKIIδ-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Colchicine for Prevention of Post-Cardiac Surgery and Post-Pulmonary Vein Isolation Atrial Fibrillation: A Meta-Analysis.Reviews in cardiovascular medicine · 2022Pooled it
- The Deubiquitinase UCHL1 Drives Susceptibility to Atrial Fibrillation by Stabilizing CaMKII-δ.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- High levels of the cardiomyocyte-specific kinase Tnni3k impair zebrafish heart regeneration by driving chronic myocardial inflammation.bioRxiv : the preprint server for biology · 2026Article
- Multiorgan Molecular Landscape of Severe COVID-19 Revealed by Consensus Gene Signatures and RAB8B Targeting.Journal of medical virology · 2026Article
- Danhong Injection targets CaMKII through Dihydrotanshinone I to alleviate cardiomyocyte death and inflammation in viral myocarditis.Science China. Life sciences · 2026Article
- Activation of IRF3 in cardiomyocytes impairs mitochondrial oxidative function through PGC-1α inhibition and drives heart failure.Nature communications · 2026Article
- Role of the two-pore domain potassium channel TREK-1 in hyperoxia- and mechanical stretch-induced alveolar epithelial injury.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Cardiac β2 adrenergic receptor deletion drives calmodulin kinase II upregulation to induce connective tissue growth factor in cardiac fibrosis and diastolic dysfunction.Function (Oxford, England) · 2025Article
- Article
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Cardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.American journal of physiology. Heart and circulatory physiology · 2025Article
- Reversing cardiac hypertrophy and heart failure using a cardiac targeting peptide linked to miRNA106a.Clinical and translational medicine · 2025Article
- Computational modelling of cardiac fibroblast signalling reveals a key role for CaThe Journal of physiology · 2025Article
- Dysfunctional cardiomyocyte signalling and heart disease.Current opinion in cell biology · 2025Review
- Nicotine Exacerbates Arrhythmogenesis in Rabbit Right Ventricular Outflow Tract Triggered by Chronic Obstructive Pulmonary Disease.Journal of cellular and molecular medicine · 2025Article
- The Interplay Between Immunity, Inflammation and Endothelial Dysfunction.International journal of molecular sciences · 2025Review
- NLRP3 Inflammasome: A New Target for the Treatment of CVD and Depression Comorbidity.Mediators of inflammation · 2025Review
- NLRP3 inflammasome in cardiovascular diseases: an update.Frontiers in immunology · 2025Review
- Active ingredients of traditional Chinese medicine inhibit NOD-like receptor protein 3 inflammasome: a novel strategy for preventing and treating heart failure.Frontiers in immunology · 2025Review
- Heart failure, inflammation and exercise.International journal of biological sciences · 2025Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation accompanies heart failure and is a mediator of cardiac fibrosis. CaMKIIδ plays an essential role in adverse remodeling and decompensation to heart failure. We postulated that inflammation is the mechanism by which CaMKIIδ contributes to adverse remodeling in response to nonischemic interventions. We demonstrate that deletion of CaMKIIδ in the cardiomyocyte (CKO) significantly attenuates activation of NF-κB, expression of inflammatory chemokines and cytokines, and macrophage accumulation induced by angiotensin II (Ang II) infusion. The inflammasome was activated by Ang II, and this response was also diminished in CKO mice. These events occurred prior to any evidence of Ang II-induced cell death. In addition, CaMKII-dependent inflammatory gene expression and inflammasome priming were observed as early as the third hour of infusion, a time point at which macrophage recruitment was not evident. Inhibition of either the inflammasome or monocyte chemoattractant protein 1 (MCP1) signaling attenuated macrophage accumulation, and these interventions, like cardiomyocyte CaMKIIδ deletion, diminished the fibrotic response to Ang II. Thus, activation of CaMKIIδ in the cardiomyocyte represents what we believe to be a novel mechanism for initiating inflammasome activation and an inflammatory gene program that leads to macrophage recruitment and ultimately to development of fibrosis.
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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.