ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Proteasome inhibition attenuates coxsackievirus-induced myocardial damage in mice.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Combining receptor engineering and intracellular gelation for cell-based antiviral therapy against coxsackievirus B3.Journal of nanobiotechnology · 2026Article
- Cellular protein quality control in viral myocarditis: molecular mechanisms and therapeutic implication.Microbiology and molecular biology reviews : MMBR · 2025Review
- Cullin 3-mediated ubiquitination restricts enterovirus D68 replication and is counteracted by viral protease 3C.Journal of virology · 2025Article
- Mitochondrial injury and complement dysregulation are drivers of pathological inflammation in viral myocarditis.Journal of virology · 2025Article
- TRIM56 restricts Coxsackievirus B infection by mediating the ubiquitination of viral RNA-dependent RNA polymerase 3D.PLoS pathogens · 2024Article
- Infectious factors in myocarditis: a comprehensive review of common and rare pathogens.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024Review
- Role of protein Post-translational modifications in enterovirus infection.Frontiers in microbiology · 2024Review
- Viral proteases activate the CARD8 inflammasome in the human cardiovascular system.The Journal of experimental medicine · 2022Article
- Ubiquitin Carboxyl-Terminal Hydrolase L1 of Cardiomyocytes Promotes Macroautophagy and Proteostasis and Protects Against Post-myocardial Infarction Cardiac Remodeling and Heart Failure.Frontiers in cardiovascular medicine · 2022Article
- MicroRNA Modification of Coxsackievirus B3 Decreases Its Toxicity, while Retaining Oncolytic Potency against Lung Cancer.Molecular therapy oncolytics · 2020Article
- The Capsid Protein VP1 of Coxsackievirus B Induces Cell Cycle Arrest by Up-Regulating Heat Shock Protein 70.Frontiers in microbiology · 2019Article
- Label-Free Digital Holo-tomographic Microscopy Reveals Virus-Induced Cytopathic Effects in Live Cells.mSphere · 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
- Phosphorylation and degradation of αB-crystallin during enterovirus infection facilitates viral replication and induces viral pathogenesis.Oncotarget · 2017Article
- PA28 modulates antigen processing and viral replication during coxsackievirus B3 infection.PloS one · 2017Article
- Cardiac Gab1 deletion leads to dilated cardiomyopathy associated with mitochondrial damage and cardiomyocyte apoptosis.Cell death and differentiation · 2016Article
- Cytoplasmic translocation, aggregation, and cleavage of TDP-43 by enteroviral proteases modulate viral pathogenesis.Cell death and differentiation · 2015Article
- Intricacies of cardiac damage in coxsackievirus B3 infection: implications for therapy.International journal of cardiology · 2014Review
- Dominant-negative function of the C-terminal fragments of NBR1 and SQSTM1 generated during enteroviral infection.Cell death and differentiation · 2014Article
- Altered ubiquitin-proteasome signaling in right ventricular hypertrophy and failure.American journal of physiology. Heart and circulatory physiology · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coxsackievirus B3 (CVB3) is one of the most prevalent pathogens of viral myocarditis, which may persist chronically and progress to dilated cardiomyopathy. We previously demonstrated a critical role of the ubiquitin-proteasome system (UPS) in the regulation of coxsackievirus replication in mouse cardiomyocytes. In the present study, we extend our interest to an in vivo animal model to examine the regulation and role of the UPS in CVB3-induced murine myocarditis. Male myocarditis-susceptible A/J mice at age 4-5 wk were randomized to four groups: sham infection + vehicle (n = 10), sham infection + proteasome inhibitor (n = 10), virus + vehicle (n = 20), and virus + proteasome inhibitor (n = 20). Proteasome inhibitor was administered subcutaneously once a day for 3 days. Mice were killed on day 9 after infection, and infected hearts were harvested for Western blot analysis, plaque assay, immunostaining, and histological examination. We showed that CVB3 infection led to an accumulation of ubiquitin conjugates at 9 days after infection. Protein levels of ubiquitin-activating enzyme E1A/E1B, ubiquitin-conjugating enzyme UBCH7, as well as deubiquitinating enzyme UCHL1 were markedly increased in CVB3-infected mice compared with sham infection. However, there was no significant alteration in proteasome activities at 9 days after infection. Immunohistochemical staining revealed that increased expression of E1A/E1B was mainly localized to virus-damaged cells. Finally, we showed that application of a proteasome inhibitor significantly reduced CVB3-induced myocardial damage. This observation reveals a novel mechanism of coxsackieviral pathogenesis, and suggests that the UPS may be an attractive therapeutic target against coxsackievirus-induced myocarditis.
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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.