ArticleJournal of the American Heart Association2014
Tenascin-C aggravates autoimmune myocarditis via dendritic cell activation and Th17 cell differentiation.
Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 75 citations in OpenAlex.
- Targeting Autoimmune Myocarditis with Lemon Balm Extract: In Vivo Molecular Approach.International journal of molecular sciences · 2026Article
- IFITM1 is required for epithelial mesenchymal transition in airway remodeling of allergic asthma.The World Allergy Organization journal · 2026Article
- ITGAX promotes Th17-cell differentiation and drives pathogenesis in pediatric ulcerative colitis.Histology and histopathology · 2026Article
- Preclinical mouse models of immune checkpoint inhibitor-associated myocarditis.Nature cardiovascular research · 2025Review
- Review
- Coronavirus disease 2019-related myocarditis genes contribute to ECMO prognosis.BMC cardiovascular disorders · 2024Article
- Targeting myocardial inflammation: investigating the therapeutic potential of atrial natriuretic peptide in atrial fibrosis.Molecular biology reports · 2024Article
- Biology of Tenascin C and its Role in Physiology and Pathology.Current medicinal chemistry · 2024Review
- Fulminant myocarditis associated with human rhinovirus A66 infection: a case report.Frontiers in pediatrics · 2024Article
- New drug discovery of cardiac anti-arrhythmic drugs: insights in animal models.Scientific reports · 2023Article
- Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κB signaling pathway.Iranian journal of basic medical sciences · 2023Article
- Tenascin-C: A Key Regulator in Angiogenesis during Wound Healing.Biomolecules · 2022Review
- Advances on the roles of tenascin-C in cancer.Journal of cell science · 2022Article
- Tenascin-C in fibrosis in multiple organs: Translational implications.Seminars in cell & developmental biology · 2022Review
- Sinus Node Dysfunction Co-occurring with Immune Checkpoint Inhibitor-associated Myocarditis.Internal medicine (Tokyo, Japan) · 2022Article
- Animal Models to Study Cardiac Arrhythmias.Circulation research · 2022Review
- Tenascin-C is a driver of inflammation in the DSS model of colitis.Matrix biology plus · 2022Article
- Tenascin-C induction exacerbates post-stroke brain damage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- The Role of Matrix Proteins in Cardiac Pathology.International journal of molecular sciences · 2022Review
- Integrated Single-Cell and RNA Sequencing Analysis Identifies Key Immune Cell and Dendritic Cells Associated Genes Participated in Myocarditis.Journal of immunology research · 2022Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTenascin-C (TN-C), an extracellular matrix glycoprotein, appears at several important steps of cardiac development in the embryo, but is sparse in the normal adult heart. TN-C re-expresses under pathological conditions including myocarditis, and is closely associated with tissue injury and inflammation in both experimental and clinical settings. However, the pathophysiological role of TN-C in the development of myocarditis is not clear. We examined how TN-C affects the initiation of experimental autoimmune myocarditis, immunologically. METHODS AND
resultsA model of experimental autoimmune myocarditis was established in BALB/c mice by immunization with murine α-myosin heavy chains. We found that TN-C knockout mice were protected from severe myocarditis compared to wild-type mice. TN-C induced synthesis of proinflammatory cytokines, including interleukin (IL)-6, in dendritic cells via activation of a Toll-like receptor 4, which led to T-helper (Th)17 cell differentiation and exacerbated the myocardial inflammation. In the transfer experiment, dendritic cells loaded with cardiac myosin peptide acquired the functional capacity to induce myocarditis when stimulated with TN-C; however, TN-C-stimulated dendritic cells generated from Toll-like receptor 4 knockout mice did not induce myocarditis in recipients.
conclusionsOur results demonstrated that TN-C aggravates autoimmune myocarditis by driving the dendritic cell activation and Th17 differentiation via Toll-like receptor 4. The blockade of Toll-like receptor 4-mediated signaling to inhibit the proinflammatory effects of TN-C could be a promising therapeutic strategy against autoimmune myocarditis.
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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.