ArticleJournal of biomedical science2024
Targeting NLRP3 signaling reduces myocarditis-induced arrhythmogenesis and cardiac remodeling.
Article in Journal of biomedical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Cardioimmunology of Myocarditis: Targeting the IL-1 Pathway.Current cardiology reports · 2026Review
- Heart-Type Fatty Acid-Binding Protein (H-FABP) as a Candidate Adjunctive Biomarker for Immune Checkpoint Inhibitor-Related Cardiotoxicity: Linking Early Immune-Metabolic Myocardial Injury with Translational Cardio-Oncology.International journal of molecular sciences · 2026Review
- Evidence of Cardiotoxic Immune Activation by Triple Immune Checkpoint Blockade: A Translational Alert for Clinical Surveillance in Patients With Cancer.Journal of cardiovascular pharmacology · 2026Article
- Inflammasomes as Potential Therapeutic Targets to Prevent Chronic Active Viral Myocarditis-Translating Basic Science into Clinical Practice.International journal of molecular sciences · 2025Review
- Article
- Inhibitors of the Interleukin-1 Receptor Accessory Protein Signaling: Another Asset in the Cardio-Immunology Toolbox.Circulation. Heart failure · 2024Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundMyocarditis substantially increases the risk of ventricular arrhythmia. Approximately 30% of all ventricular arrhythmia cases in patients with myocarditis originate from the right ventricular outflow tract (RVOT). However, the role of NLRP3 signaling in RVOT arrhythmogenesis remains unclear.
methodsRats with myosin peptide-induced myocarditis (experimental group) were treated with an NLRP3 inhibitor (MCC950; 10 mg/kg, daily for 14 days) or left untreated. Then, they were subjected to electrocardiography and echocardiography. Ventricular tissue samples were collected from each rat's RVOT, right ventricular apex (RVA), and left ventricle (LV) and examined through conventional microelectrode and histopathologic analyses. In addition, whole-cell patch-clamp recording, confocal fluorescence microscopy, and Western blotting were performed to evaluate ionic currents, intracellular Ca
resultsThe LV ejection fraction was lower and premature ventricular contraction frequency was higher in the experimental group than in the control group (rats not exposed to myosin peptide). Myocarditis increased the infiltration of inflammatory cells into cardiac tissue and upregulated the expression of NLRP3; these observations were more prominent in the RVOT and RVA than in the LV. Furthermore, experimental rats treated with MCC950 (treatment group) improved their LV ejection fraction and reduced the frequency of premature ventricular contraction. Histopathological analysis revealed higher incidence of abnormal automaticity and pacing-induced ventricular tachycardia in the RVOTs of the experimental group than in those of the control and treatment groups. However, the incidences of these conditions in the RVA and LV were similar across the groups. The RVOT myocytes of the experimental group exhibited lower Ca
conclusionMyocarditis may increase the rate of RVOT arrhythmogenesis, possibly through electrical and structural remodeling. These changes may be mitigated by inhibiting NLRP3 signaling.
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