ArticleScientific reports2017
Transmissible endoplasmic reticulum stress from myocardiocytes to macrophages is pivotal for the pathogenesis of CVB3-induced viral myocarditis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 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
- Ceramide mediates cell-to-cell ER stress transmission by modulating membrane fluidity.The Journal of cell biology · 2025Article
- Neurogenic differentiation 2 promotes inflammatory activation of macrophages in doxorubicin-induced myocarditis via regulating protein kinase D.BMC cardiovascular disorders · 2025Article
- Review
- Coxsackievirus group B3 regulates ASS1-mediated metabolic reprogramming and promotes macrophage inflammatory polarization in viral myocarditis.Journal of virology · 2024Article
- Article
- Immunopathogenesis and immunomodulatory therapy for myocarditis.Science China. Life sciences · 2023Review
- Endoplasmic reticulum stress mediates the myeloid-derived immune suppression associated with cancer and infectious disease.Journal of translational medicine · 2023Review
- Exploring the role of T helper subgroups and their cytokines in the development of pregnancy-induced hypertension.Frontiers in immunology · 2023Article
- Endoplasmic reticulum-stress and unfolded protein response-activation in immune-mediated necrotizing myopathy.Brain pathology (Zurich, Switzerland) · 2022Article
- Transmissible ER stress between macrophages and tumor cells configures tumor microenvironment.Cellular and molecular life sciences : CMLS · 2022Article
- Review
- Systematic Exploration in Tissue-Pathway Associations of Complex Traits Using Comprehensive eQTLs Catalog.Frontiers in big data · 2021Article
- An Albumin-Binding Domain Peptide Confers Enhanced Immunoprotection Against Viral Myocarditis by CVB3 VP1 Vaccine.Frontiers in immunology · 2021Article
- lncRNA AK085865 Promotes Macrophage M2 Polarization in CVB3-Induced VM by Regulating ILF2-ILF3 Complex-Mediated miRNA-192 Biogenesis.Molecular therapy. Nucleic acids · 2020Article
- NOD1 and NOD2 Activation by Diverse Stimuli: a Possible Role for Sensing Pathogen-Induced Endoplasmic Reticulum Stress.Infection and immunity · 2020Review
- ER stress activates immunosuppressive network: implications for aging and Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Roles and Mechanisms of Interleukin-12 Family Members in Cardiovascular Diseases: Opportunities and Challenges.Frontiers in pharmacology · 2020Review
- Inhibitory effect of melatonin on Mst1 ameliorates myocarditis through attenuating ER stress and mitochondrial dysfunction.Journal of molecular histology · 2019Article
- Endoplasmic reticulum stress is transmissible in vitro between cells of the central nervous system.Journal of neurochemistry · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infiltrating macrophages have been proven as a pivotal pathological inflammatory cell subset in coxsackievirus B3 (CVB3) induced viral myocarditis. However, the mechanisms underlying the initiation and promotion of macrophage pro-inflammatory responses are still blur. We previously reported that cardiac ER stress contributed to CVB3-induced myocarditis by augmenting inflammation. In this study, we focused on the influence of ER stress on the macrophage inflammatory responses in the viral myocarditis. We found that ER stress was robustly induced in the cardiac infiltrating macrophages from CVB3-infected mice, and robustly facilitated the production of pro-inflammatory cytokines (IL-6, IL-12, MCP-1 and IP-10). Consistently, adoptive transfer of ER stressed macrophages significantly worsened the viral myocarditis; while transfer of ER stress-inhibited macrophages obviously alleviated the myocarditis. To our surprise, this significantly activated ER stress was not directly caused by the virus stimulation, but was transferred from the CVB3-infected, ER stressed myocardiocytes via soluble molecules in a TLR2, 4-independent way. In the present study, we reported that the transmissible ER stress from the infected myocardiocytes to macrophages could augment the pro-inflammatory responses and promoted the pathogenesis of viral myocarditis. Blocking ER stress transmission, instead of inhibiting its initiation, may represent novel therapeutic strategies against viral myocarditis.
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