ArticleInternational journal of cardiology2016
Dual roles of calpain in facilitating Coxsackievirus B3 replication and prompting inflammation in acute myocarditis.
Article in International journal of cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting the Myocardial Microenvironment: Novel Antiviral Strategies and Therapeutic Perspectives for Coxsackievirus B-Induced Myocarditis.Journal of the American Heart Association · 2026Review
- Integrated Transcriptomic Analyses and Experimental Validation Identify TSPO as a Mitochondria-Associated Therapeutic Target in Myocarditis.Mediators of inflammation · 2026Article
- Inhibition of calpain reduces cell apoptosis by suppressing mitochondrial fission in acute viral myocarditis.Cell biology and toxicology · 2022Article
- Advances in cell death mechanisms involved in viral myocarditis.Frontiers in cardiovascular medicine · 2022Review
- Targeted inhibition of calpain in mitochondria alleviates oxidative stress-induced myocardial injury.Acta pharmacologica Sinica · 2021Article
- Deletion of P110δ promotes the development of myocarditis in ApoE‑deficient mice by increasing mononuclear cell peritoneal infiltration.Molecular medicine reports · 2020Article
- Letter to the Editor in response to the article "Could IL-17 represent a new therapeutic target for the treatment and/or management of COVID-19-related respiratory syndrome?"Pharmacological research · 2020Article
- Picornavirus Cellular Remodeling: Doubling Down in Response to Viral-Induced Inflammation.Current clinical microbiology reports · 2020Article
- Inhibition of calpain alleviates coxsackievirus B3-induced myocarditis through suppressing the canonical NLRP3 inflammasome/caspase-1-mediated and noncanonical caspase-11-mediated pyroptosis pathways.American journal of translational research · 2020Article
- The protective role of microRNA-21 against coxsackievirus B3 infection through targeting the MAP2K3/P38 MAPK signaling pathway.Journal of translational medicine · 2019Article
- Cardiac Proteome Profiling in Ischemic and Dilated Cardiomyopathy Mouse Models.Frontiers in physiology · 2019Article
- AIM2 Co-immunization with VP1 Is Associated with Increased Memory CD8 T Cells and Mounts Long Lasting Protection against Coxsackievirus B3 Challenge.Frontiers in cellular and infection microbiology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundViral myocarditis (VMC) treatment has long been lacking of effective methods. Our former studies indicated roles of calpain in VMC pathogenesis. This study aimed at verifying the potential of calpain in Coxsackievirus B3 (CVB3)-induced myocarditis treatment.
methodsA transgenic mouse overexpressing the endogenous calpain inhibitor, calpastatin, was introduced in the study. VMC mouse model was established via intraperitoneal injection of CVB3 in transgenic and wild mouse respectively. Myocardial injury was assayed histologically (HE staining and pathology grading) and serologically (myocardial damage markers of CK-MB and cTnI). CVB3 replication was observed in vivo and in vitro via the capsid protein VP1 detection or virus titration. Inflammation/fibrotic factors of MPO, perforin, IFNγ, IL17, Smad3 and MMP2 were evaluated using western blot or immunohistology stain. Role of calpain in regulating fibroblast migration was studied in scratch assays.
resultsCalpastatin overexpression ameliorated myocardial injury induced by CVB3 infection significantly in transgenic mouse indicated by reduced peripheral CK-MB and cTnI levels and improved histology injury. Comparing with CVB3-infected wild type mouse, the transgenic mouse heart tissue carried lower virus load. The inflammation factors of MPO, perforin, IFNγ and IL17 were down-regulated accompanied with fibrotic agents of Smad3 and MMP2 inhibition. And calpain participated in the migration of fibroblasts in vitro, which further proves its role in regulating fibrosis.
conclusionCalpain plays dual roles of facilitating CVB3 replication and inflammation promotion. Calpain inhibition in CVB3-induced myocarditis showed significant treatment effect. Calpain might be a novel target for VMC treatment in clinical practices.
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