ArticleMediators of inflammation2014
Cardiac fibroblasts aggravate viral myocarditis: cell specific coxsackievirus B3 replication.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- Targeting the Myocardial Microenvironment: Novel Antiviral Strategies and Therapeutic Perspectives for Coxsackievirus B-Induced Myocarditis.Journal of the American Heart Association · 2026Review
- Pediatric viral myocarditis: mechanisms, experimental models, and research gaps.Pediatric research · 2026Review
- Human Primary Macrophages Can Transmit Coxsackie B4 Virus to Pancreatic Cells In Vitro.Journal of medical virology · 2024Article
- Three modes of viral adaption by the heart.Science advances · 2024Article
- Article
- Ferroptosis in diabetic cardiomyopathy: Advances in cardiac fibroblast-cardiomyocyte interactions.Heliyon · 2024Review
- Three Modes of Viral Adaption by the Heart.bioRxiv : the preprint server for biology · 2024Article
- GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome.Nature cardiovascular research · 2024Article
- Review
- Dissecting the cellular landscape and transcriptome network in viral myocarditis by single-cell RNA sequencing.iScience · 2022Article
- Cardiac SARS-CoV-2 infection is associated with pro-inflammatory transcriptomic alterations within the heart.Cardiovascular research · 2022Article
- Mechanisms and Therapeutic Strategies of Viral Myocarditis Targeting Autophagy.Frontiers in pharmacology · 2022Review
- The Roles of Cardiac Fibroblasts and Endothelial Cells in Myocarditis.Frontiers in cardiovascular medicine · 2022Review
- Human cardiac fibroblasts produce pro-inflammatory cytokines upon TLRs and RLRs stimulation.Molecular and cellular biochemistry · 2021Article
- Cell type-specific roles of PAR1 in Coxsackievirus B3 infection.Scientific reports · 2021Article
- Review
- Article
- Modulation of the acute defence reaction by eplerenone prevents cardiac disease progression in viral myocarditis.ESC heart failure · 2020Article
- What Is the Role of the Inflammation in the Pathogenesis of Heart Failure?Current cardiology reports · 2020Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocarditis is an inflammatory disease caused by viral infection. Different subpopulations of leukocytes enter the cardiac tissue and lead to severe cardiac inflammation associated with myocyte loss and remodeling. Here, we study possible cell sources for viral replication using three compartments of the heart: fibroblasts, cardiomyocytes, and macrophages. We infected C57BL/6j mice with Coxsackievirus B3 (CVB3) and detected increased gene expression of anti-inflammatory and antiviral cytokines in the heart. Subsequently, we infected cardiac fibroblasts, cardiomyocytes, and macrophages with CVB3. Due to viral infection, the expression of TNF-α, IL-6, MCP-1, and IFN-β was significantly increased in cardiac fibroblasts compared to cardiomyocytes or macrophages. We found that in addition to cardiomyocytes cardiac fibroblasts were infected by CVB3 and displayed a higher virus replication (132-fold increase) compared to cardiomyocytes (14-fold increase) between 6 and 24 hours after infection. At higher virus concentrations, macrophages are able to reduce the viral copy number. At low virus concentration a persistent virus infection was determined. Therefore, we suggest that cardiac fibroblasts play an important role in the pathology of CVB3-induced myocarditis and are another important contributor of virus replication aggravating myocarditis.
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Registered trials
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