ArticleThe Journal of clinical investigation1996
Identification of cardiac myosin peptides capable of inducing autoimmune myocarditis in BALB/c mice.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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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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.
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Who cites it
79 citing papers in PubMed, 203 citations in OpenAlex.
- Heart-specific T cell responses: from antigens to disease mechanisms.Nature reviews. Cardiology · 2026Review
- Article
- Myosin-Specific T Cells at the Heart of Myocardial Pathophysiology.JACC. Basic to translational science · 2026Article
- Crocins Ameliorate Experimental Immune Checkpoint Inhibitor-Related Myocarditis by Targeting the Hpx/Nrf2/HO-1 Pathway.International journal of molecular sciences · 2026Article
- Combined Adaptive Immune Mechanisms Mediate Cardiac Injury After COVID-19 Vaccination.Circulation · 2025Article
- Pathogenic drivers of lupus myocarditis and potential therapeutic targets.Experimental & molecular medicine · 2025Review
- Cardiac Troponin I Antibodies Induce Cardiomyocyte Damage and Alter Cell Morphology.International journal of molecular sciences · 2025Article
- Preclinical mouse models of immune checkpoint inhibitor-associated myocarditis.Nature cardiovascular research · 2025Review
- T cells in cardiac health and disease.The Journal of clinical investigation · 2025Review
- The role of eosinophils and their activation state in hypereosinophilia-associated heart disease.Frontiers in immunology · 2025Article
- Modeling immune checkpoint inhibitor associated myocarditisJournal of molecular and cellular cardiology plus · 2024Article
- Anti-CTLA-4 m2a Antibody Exacerbates Cardiac Injury in Experimental Autoimmune Myocarditis Mice By Promoting Ccl5-Neutrophil Infiltration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Immune-checkpoint inhibitor-mediated myocarditis: CTLA4, PD1 and LAG3 in the heart.Nature reviews. Cancer · 2024Review
- Non-Canonical Localization of Cardiac Troponins: Expanding Functions or Causing Pathologies?International journal of molecular sciences · 2024Review
- Immune checkpoint inhibitors break whose heart? Perspectives from cardio-immuno-oncology.Genes & diseases · 2024Review
- New drug discovery of cardiac anti-arrhythmic drugs: insights in animal models.Scientific reports · 2023Article
- Article
- Cardiac myosin-specific autoimmune T cells contribute to immune-checkpoint-inhibitor-associated myocarditis.Cell reports · 2022Article
- Animal Models to Study Cardiac Arrhythmias.Circulation research · 2022Review
- P2YCells · 2021Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunization with cardiac myosin induces T cell-mediated myocarditis in genetically predisposed mice and serves as a model for autoimmune heart disease. This study was undertaken to identify pathogenic epitopes on the myosin molecule. Our approach was based on the comparison of the pathogenicity between cardiac (alpha-)myosin and soleus muscle (beta-)myosin. We show that alpha-myosin is the immunodominant isoform and induces myocarditis at high severity and prevalence whereas beta-myosin induces little disease. Therefore the immunodominant epitopes of alpha-myosin must reside in regions of different amino acid sequence between alpha- and beta-myosin isoforms. Cardiac myosin peptides corresponding to these regions of difference were synthesized and tested for their ability to induce inflammatory heart disease. Three pathogenic peptides were identified. One peptide that is located in the head portion of the molecule induced severe myocarditis, whereas two others that reside in the rod portion possessed only minor pathogenicity. The identification of pathogenic epitopes on the cardiac myosin molecule will allow detailed studies on the recognition of this antigen by the immune system and might be used to downmodulate ongoing heart disease.
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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.