ArticleJournal of cardiac failure2009
Cardiac cell-specific apoptotic and cytokine responses to reovirus infection: determinants of myocarditic phenotype.
Article in Journal of cardiac failure, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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
6 citing papers in PubMed, 7 citations in OpenAlex.
- Spatiotemporal transcriptomics reveals pathogenesis of viral myocarditis.Nature cardiovascular research · 2022Article
- NF-κB activation is cell type-specific in the heart.Virology · 2017Article
- Viral myocarditis: from experimental models to molecular diagnosis in patients.Heart failure reviews · 2013Review
- Critical role for death-receptor mediated apoptotic signaling in viral myocarditis.Journal of cardiac failure · 2010Article
- Interferon regulatory factor 3 attenuates reovirus myocarditis and contributes to viral clearance.Journal of virology · 2010Article
- Proteomic analysis reveals virus-specific Hsp25 modulation in cardiac myocytes.Journal of proteome research · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe pathophysiologic mechanisms underlying viral myocarditis are not well defined. As a result, effective treatments do not exist and viral myocarditis remains a potentially lethal infection of the heart. METHODS AND
resultsWe used cultured rat cardiac myocytes and fibroblasts to investigate apoptosis and cytokine production in response to infection by myocarditic vs. non-myocarditic strains of reovirus. Myocarditic reovirus strain 8B and non-myocarditic strain DB188 replicate comparably in each cardiac cell type. However, strain 8B and related myocarditic reoviruses preferentially increase apoptosis of myocytes relative to fibroblasts, whereas DB188 and nonmyocarditic strains preferentially increase fibroblast apoptosis. Infection of cardiac fibroblasts with the nonmyocarditic strain DB188 elicits substantial increases in a panel of cytokines compared to fibroblasts infected with strain 8B or mock-infected controls. Analysis of culture supernatants using cytometric bead arrays revealed that DB188 enhanced release of interleukin (IL)-1beta, IL-4, IL-6, IL-10, IL-12(p70), GRO-KC, tumor necrosis factor-alpha, and MCP-1 relative to 8B or mock-infected controls (all P < .05).
conclusionWe hypothesize that differential cytokine production and cell-specific apoptosis are important determinants of myocarditic potential of reoviral strains. Therapies that target the beneficial effects of cytokines in limiting cytopathic damage may offer an effective and novel treatment approach to viral myocarditis.
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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.