ArticleThe American journal of pathology2006
Ongoing coxsackievirus myocarditis is associated with increased formation and activity of myocardial immunoproteasomes.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 56 citations in OpenAlex.
- Cellular protein quality control in viral myocarditis: molecular mechanisms and therapeutic implication.Microbiology and molecular biology reviews : MMBR · 2025Review
- Spatiotemporal transcriptomics reveals pathogenesis of viral myocarditis.Nature cardiovascular research · 2022Article
- Review
- Induction of Proteasome Subunit Low Molecular Weight Protein (LMP)-2 Is Required to Induce Active Remodeling in Adult Rat Ventricular Cardiomyocytes.Medical sciences (Basel, Switzerland) · 2020Article
- Article
- Protein modification with ISG15 blocks coxsackievirus pathology by antiviral and metabolic reprogramming.Science advances · 2020Article
- Targeting Protein Kinase G to Treat Cardiac Proteotoxicity.Frontiers in physiology · 2020Review
- Proteasomes and Several Aspects of Their Heterogeneity Relevant to Cancer.Frontiers in oncology · 2019Review
- The immunoproteasome-specific inhibitor ONX 0914 reverses susceptibility to acute viral myocarditis.EMBO molecular medicine · 2018Article
- Silencing the CSF-1 Axis Using Nanoparticle Encapsulated siRNA Mitigates Viral and Autoimmune Myocarditis.Frontiers in immunology · 2018Article
- Proteasomal Protein Degradation: Adaptation of Cellular Proteolysis With Impact on Virus-and Cytokine-Mediated Damage of Heart Tissue During Myocarditis.Frontiers in immunology · 2018Review
- PA28 modulates antigen processing and viral replication during coxsackievirus B3 infection.PloS one · 2017Article
- Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis.Journal of immunology research · 2017Article
- Interferon-dependent immunoproteasome activity during mouse adenovirus type 1 infection.Virology · 2016Article
- Targeting the ubiquitin-proteasome system in heart disease: the basis for new therapeutic strategies.Antioxidants & redox signaling · 2014Review
- Bioinformatics multivariate analysis determined a set of phase-specific biomarker candidates in a novel mouse model for viral myocarditis.Circulation. Cardiovascular genetics · 2014Article
- PAR-1 contributes to the innate immune response during viral infection.The Journal of clinical investigation · 2013Article
- Cytokine-induced oxidative stress in cardiac inflammation and heart failure-how the ubiquitin proteasome system targets this vicious cycle.Frontiers in physiology · 2013Article
- Interferon-γ causes cardiac myocyte atrophy via selective degradation of myosin heavy chain in a model of chronic myocarditis.The American journal of pathology · 2012Article
- Proteome dynamics and proteome function of cardiac 19S proteasomes.Molecular & cellular proteomics : MCP · 2011Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing body of evidence indicates that viral infections of the heart contribute to ongoing myocarditis and dilated cardiomyopathy. Murine models of coxsackievirus B3 (CVB3)-induced myocarditis mimic the human disease and allow identification of susceptibility factors that modulate the course of viral myocarditis. Susceptible mouse strains develop chronic myocarditis on the basis of restricted viral replication, whereas resistant strains recover after successful virus elimination. In comparative whole-genome microarray analyses of infected hearts, several genes involved in the processing and presentation of viral epitopes were found to be uniformly up-regulated in acutely CVB3-infected susceptible mice compared with resistant animals. In particular, expression of the catalytic subunits LMP2, LMP7, and MECL-1, immunoproteasome proteins important in the generation of major histocom-patibility complex (MHC) class I-restricted peptides, was clearly enhanced in the susceptible host. Increased expression resulted in enhanced formation of immunoproteasomes and altered proteolytic activities of proteasomes in the heart. This was accompanied by a concerted up-regulation of the antigen-presenting machinery in susceptible mice. Thus, we propose that increased formation of immunoproteasomes in susceptible mice affects the generation of antigenic peptides and the subsequent T-cell-mediated immune responses.
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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.