ArticleAutoimmunity2008
Consequences of unlocking the cardiac myosin molecule in human myocarditis and cardiomyopathies.
Article in Autoimmunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
49 citing papers in PubMed, 78 citations in OpenAlex.
- Interpretable AI model reveals spatial codes of cell recruitment in tissues.Nature biomedical engineering · 2026Article
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Agonistic autoantibodies targeting AT1R and ETAR: Mechanistic insights and emerging implications in cardiovascular disease.Journal of translational autoimmunity · 2026Article
- Autoantibody Profiling in Cardiomyopathies: Toward Immune-Guided Risk Stratification and Therapy.Journal of clinical medicine · 2026Review
- Cardioprotective Effect of Metformin Treatment in Mouse Model of Experimental Autoimmune Myocarditis.Cardiovascular therapeutics · 2026Article
- A human-on-human assay for detecting anti-myocardial antibodies in patients with myocardial disease.Frontiers in immunology · 2026Article
- An Interpretable Multi-instance Learner Decodes Cellular Recruitment from Spatially Resolved Transcriptomics.bioRxiv : the preprint server for biology · 2025Article
- Preclinical mouse models of immune checkpoint inhibitor-associated myocarditis.Nature cardiovascular research · 2025Review
- Cardiac autoantibodies promote a fibrotic transcriptome and reduced ventricular recovery in human myocarditis.Frontiers in immunology · 2025Article
- Engineered human heart tissue reveals pathogenicity of autoantibodies in systemic lupus erythematosus.Nature cardiovascular research · 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
- RhoA/ROCK Pathway Is Upregulated in Experimental Autoimmune Myocarditis and Is Inhibited by Simvastatin at the Stage of Myosin Light Chain Phosphorylation.Biomedicines · 2024Article
- Unraveling the Uncommon: A Case Report of Giant Cell Myocarditis and Examination of Existing Literature.The American journal of case reports · 2024Review
- The knowns and unknowns of cardiac autoimmunity in viral myocarditis.Reviews in medical virology · 2023Review
- Article
- Mediators and mechanisms of immune checkpoint inhibitor-associated myocarditis: Insights from mouse and human.Immunological reviews · 2023Review
- COVID-19-Induced Myocarditis: Pathophysiological Roles of ACE2 and Toll-like Receptors.International journal of molecular sciences · 2023Review
- Comparison of COVID-19 Vaccine-Associated Myocarditis and Viral Myocarditis Pathology.Vaccines · 2023Review
- Review
- Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Myocarditis, often initiated by viral infection, may progress to autoimmune inflammatory heart disease, dilated cardiomyopathy and heart failure. Although cardiac myosin is a dominant autoantigen in animal models of myocarditis and is released from the heart during viral myocarditis, the characterization, role and significance of anti-cardiac myosin autoantibodies is poorly defined. In our study, we define the human cardiac myosin epitopes in human myocarditis and cardiomyopathies and establish a mechanism to explain how anti-cardiac myosin autoantibodies may contribute to heart disease. We show that autoantibodies to cardiac myosin in sera from myocarditis and dilated cardiomyopathies in humans targeted primarily epitopes in the S2 hinge region of cardiac myosin. In addition, anti-cardiac myosin antibodies in sera or purified IgG from myocarditis and cardiomyopathy targeted the beta-adrenergic receptor and induced antibody-mediated cAMP-dependent protein kinase A (PKA) cell signaling activity in heart cells. Antibody-mediated PKA activity in sera was abrogated by absorption with anti-human IgG. Antibody-mediated cell signaling of PKA was blocked by antigen-specific inhibition by human cardiac myosin or the beta-adrenergic receptor but not the alpha adrenergic receptor or bovine serum albumin. Propranolol, a beta blocker and inhibitor of the beta-adrenergic receptor pathway also blocked the antibody-mediated signaling of the beta-adrenergic receptor and PKA. The data suggest that IgG antibody against human cardiac myosin reacts with the beta-adrenergic receptor and triggers PKA signaling in heart cells. In summary, we have identified a new class of crossreactive autoantibodies against human cardiac myosin and the beta-adrenergic receptor in the heart. In addition, we have defined disease specific peptide epitopes in the human cardiac myosin rod S2 region in human myocarditis and cardiomyopathy as well as a mechanistic role of autoantibody in the pathogenesis of disease.
Indexed as
Identifiers
What OpenQuestion holds
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.