ArticlePLoS pathogens2018
Cathepsin B aggravates coxsackievirus B3-induced myocarditis through activating the inflammasome and promoting pyroptosis.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 96 citations in OpenAlex.
- 3C suppresses PINK1-mediated mitophagy and contributes to coxsackievirus B3 replication.Virulence · 2026Article
- Suppression of Calpain Attenuates Coxsackievirus B3-Induced Myocarditis by Regulating RIPK1/RIPK3/MLKL Pathway.Journal of cardiovascular translational research · 2026Article
- Dissecting myocardial and systemic drivers of cardiac dysfunction in the murine CVB3 myocarditis model using microRNA-guided viral detargeting.Basic research in cardiology · 2026Article
- Long noncoding RNA#61 synergizes with viral PA-X to augment pyroptosis and attenuate the virulence of highly pathogenic H5N1 influenza virus in mice.Journal of virology · 2026Article
- Gasdermin D-dependent neutrophil pyroptosis exacerbates Coxsackievirus A6-induced neuroinflammation through NET formation.Journal of neuroinflammation · 2026Article
- Integrated bioinformatics and network search identify biomarkers and comorbid mechanisms of atrial fibrillation and ischemic stroke.Medicine · 2026Article
- BACH2 alleviates immune checkpoint inhibitors-induced cardiac pyroptosis via transcriptionally promoting GRSF1.Clinical and translational medicine · 2026Article
- Article
- NLRP3-mediated pyroptosis in cardiovascular disease: from molecular mechanisms to therapeutic targets.Frontiers in pharmacology · 2026Review
- Review
- Cathepsin B in human peripheral blood lymphocytes as a peripheral biomarker for cardiac hypertrophy.Scientific reports · 2025Article
- Cathepsin B Levels Correlate with the Severity of Canine Myositis.Biomolecules · 2025Article
- Pentraxin 3 promotes the expression of pro-inflammatory cytokines and the migration of macrophages in myocarditis.BMC cardiovascular disorders · 2025Article
- Neurogenic differentiation 2 promotes inflammatory activation of macrophages in doxorubicin-induced myocarditis via regulating protein kinase D.BMC cardiovascular disorders · 2025Article
- Non-coding RNAs affecting NLRP3 inflammasome pathway in diabetic cardiomyopathy: a comprehensive review of potential therapeutic options.Journal of translational medicine · 2025Review
- Underlying Mechanism of Lysosomal Membrane Permeabilization in CNS Injury: A Literature Review.Molecular neurobiology · 2025Review
- Comprehensive Analysis of Differences in N6-Methyladenosine RNA Methylation Groups in CVB3-Induced Viral Myocarditis and Identification of the Anti-Apoptotic Role of RBM15B.Journal of inflammation research · 2025Article
- Identification of Cardiometabolic Protein Biomarkers for Acute Myocardial Infarction Using Olink Proteomics.Journal of inflammation research · 2025Article
- Active ingredients of traditional Chinese medicine inhibit NOD-like receptor protein 3 inflammasome: a novel strategy for preventing and treating heart failure.Frontiers in immunology · 2025Review
- Shikonin fromAnnals of medicine · 2024Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cathepsin B (CatB) is a cysteine proteolytic enzyme widely expressed in various cells and mainly located in the lysosomes. It contributes to the pathogenesis and development of many diseases. However, the role of CatB in viral myocarditis (VMC) has never been elucidated. Here we generated the VMC model by intraperitoneal injection of coxsackievirus B3 (CVB3) into mice. At day 7 and day 28, we found CatB was significantly activated in hearts from VMC mice. Compared with the wild-type mice receiving equal amount of CVB3, genetic ablation of CatB (Ctsb-/-) significantly improved survival, reduced inflammatory cell infiltration, decreased serum level of cardiac troponin I, and ameliorated cardiac dysfunction, without altering virus titers in hearts. Conversely, genetic deletion of cystatin C (Cstc-/-), which markedly enhanced CatB levels in hearts, distinctly increased the severity of VMC. Furthermore, compared with the control, we found the inflammasome was activated in the hearts of wild-type mice with VMC, which was attenuated in the hearts of Ctsb-/- mice but was further enhanced in Cstc-/- mice. Consistently, the inflammasome-initiated pyroptosis was reduced in Ctsb-/- mice hearts and further increased in Cstc-/- mice. These results suggest that CatB aggravates CVB3-induced VMC probably through activating the inflammasome and promoting pyroptosis. This finding might provide a novel strategy for VMC treatment.
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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.