ArticleJournal of cardiac failure2010
Critical role for death-receptor mediated apoptotic signaling in viral myocarditis.
Article in Journal of cardiac failure, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Differential cardiomyocyte transcriptomic remodeling during in vitro Trypanosoma cruzi infection using laboratory strains provides implications on pathogenic host responses.Tropical medicine and health · 2023Article
- TRAIL and its receptors in cardiac diseases.Frontiers in physiology · 2023Review
- The M2 Gene Is a Determinant of Reovirus-Induced Myocarditis.Journal of virology · 2022Article
- Molecular Mechanisms behind Persistent Presence of Parvovirus B19 in Human Dilated Myocardium.Advances in experimental medicine and biology · 2022Article
- The multi-functional reovirus σ3 protein is a virulence factor that suppresses stress granule formation and is associated with myocardial injury.PLoS pathogens · 2021Article
- Effects of aspartame on hsp70, bcl-2 and bax expression in immune organs of Wistar albino rats.Journal of biomedical research · 2016Article
- DNA Repair Gene Polymorphism and the Risk of Mitral Chordae Tendineae Rupture.Disease markers · 2015Article
- Viral myocarditis: from experimental models to molecular diagnosis in patients.Heart failure reviews · 2013Review
- The proapoptotic Bcl-2 protein Bax plays an important role in the pathogenesis of reovirus encephalitis.Journal of virology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundApoptosis of cardiac myocytes plays a key role in the pathogenesis of many cardiac diseases, including viral myocarditis. The apoptotic signaling pathways that are activated during viral myocarditis and the role that these pathways play in disease pathogenesis have not been clearly delineated. METHODS AND
resultsWe investigated the role of apoptotic signaling pathways after virus infection of primary cardiac myocytes. The death receptor-associated initiator caspase, caspase 8, and the effector caspase, caspase 3, were significantly activated after infection of primary cardiac myocytes with myocarditic, but not non-myocarditic, reovirus strains. Furthermore, reovirus-induced cardiac myocyte apoptosis was significantly inhibited by soluble death receptors. In contrast, the mitochondrial membrane potential remained unaltered and caspase 9, the initiator caspase associated with mitochondrial apoptotic signaling, was only weakly activated in cardiac myocytes after infection with myocarditic reovirus strains. Inhibition of mitochondrial apoptotic signaling had no effect on reovirus-induced cardiac myocyte apoptosis. In accordance with our in vitro data, caspase 8, but not caspase 9, was significantly activated in the hearts of reovirus-infected mice.
conclusionsDeath receptor, but not mitochondrial, apoptotic signaling plays a key role in apoptosis after infection of cardiac myocytes with myocarditic reovirus strains.
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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.