ArticleThe Journal of clinical investigation2002
Enhanced ERK-1/2 activation in mice susceptible to coxsackievirus-induced myocarditis.
Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 103 citations in OpenAlex.
- Cardiac tertiary immune niches drive immune activation in immune checkpoint inhibitor myocarditis.Science advances · 2026Article
- Pediatric viral myocarditis: mechanisms, experimental models, and research gaps.Pediatric research · 2026Review
- Identification of Drug Repurposing Candidates for Coxsackievirus B3 Infection in iPSC-Derived Brain-like Endothelial Cells.International journal of molecular sciences · 2025Article
- Coxsackievirus B regulates host circAKAP10 expression to promote viral replication.Archives of virology · 2025Article
- Transcriptomic analysis of coxsackievirus B3 infection in induced pluripotent stem cell-derived brain-like endothelial cells.Journal of virology · 2025Article
- Article
- Sex Differences in Expression of Pro-Inflammatory Markers and miRNAs in a Mouse Model of CVB3 Myocarditis.International journal of molecular sciences · 2024Article
- Caboxamycin Inhibits Heart Inflammation in a Coxsackievirus B3-Induced Myocarditis Mouse Model.Viruses · 2024Article
- Genetic Ablation ofBiomolecules · 2022Article
- SMAD4, activated by the TCR-triggered MEK/ERK signaling pathway, critically regulates CD8Science advances · 2022Article
- Protein Kinase B2 (PKB2/AKT2) Is Essential for Host Protection in CVB3-Induced Acute Viral Myocarditis.International journal of molecular sciences · 2022Article
- Development of Group B Coxsackievirus as an Oncolytic Virus: Opportunities and Challenges.Viruses · 2021Article
- Review
- Viral meningitis: an overview.Archives of virology · 2021Review
- Coxsackievirus B3 Infection Early in Pregnancy Induces Congenital Heart Defects Through Suppression of Fetal Cardiomyocyte Proliferation.Journal of the American Heart Association · 2021Article
- Comparison and Analysis on the Existing Single-Herbal Strategies against Viral Myocarditis.Genetics research · 2021Article
- Src-family Protein Tyrosine Kinases: A promising target for treating Cardiovascular Diseases.International journal of medical sciences · 2021Review
- Coxsackievirus Type B3 Is a Potent Oncolytic Virus againstMolecular therapy oncolytics · 2019Article
- The innate immune system in chronic cardiomyopathy: a European Society of Cardiology (ESC) scientific statement from the Working Group on Myocardial Function of the ESC.European journal of heart failure · 2018Review
- The immunoproteasome-specific inhibitor ONX 0914 reverses susceptibility to acute viral myocarditis.EMBO molecular medicine · 2018Article
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
Group B coxsackieviral (CVB) infection commonly causes viral myocarditis. Mice are protected from CVB3 myocarditis by gene-targeted knockout of p56(Lck)(Lck), the Src family kinase (Src) essential for T cell activation. Extracellular signal-regulated kinase 1 and 2 (ERK-1/2) can influence cell function downstream of Lck. Using T cell lines and neonatal cardiac myocytes we investigated the role of ERK-1/2 in CVB3 infection. In Jurkat T cells ERK-1/2 is rapidly activated by CVB3; but, this response is absent in Lck-negative JCaM T cells. Inhibition of ERK-1/2 with UO126 reduced CVB3 titers in Jurkat cells, but not in JCaM cells. In cardiac myocytes CVB3 activation of ERK-1/2 is blocked by the Src inhibitor PP2. In addition, viral production in myocytes is decreased by Src or ERK-1/2 inhibition. In vitro, in both immune and myocardial cells, ERK-1/2 is activated by CVB3 downstream of Lck and other Src's and is necessary for efficient CVB3 replication. In vivo, following CVB3 infection, ERK-1/2 activation is evident in the myocardium. ERK-1/2 activation is intense in the hearts of myocarditis-susceptible A/J mice. In contrast, significantly less ERK-1/2 activation is found in the hearts of myocarditis-resistant C57BL/6 mice. Therefore, the ERK-1/2 response to CVB3 infection may contribute to differential host susceptibility to viral myocarditis.
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