ArticleJCI insight2017
MicroRNA-125a and -b inhibit A20 and MAVS to promote inflammation and impair antiviral response in COPD.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
74 citing papers in PubMed, 114 citations in OpenAlex.
- Non-coding RNAs and RIG-I/MAVS signaling pathway: Insights for targeted therapy in influenza infection.Chinese medical journal · 2026Article
- Association of miR-146a/b and miR-181a with Chronic Obstructive Pulmonary Disease.Biochemical genetics · 2026Article
- Assessment of CFTR Dysfunction and Responsiveness to CFTR Modulators in COPD Bronchial Air-Liquid Interface Cultures.International journal of molecular sciences · 2026Article
- Review
- Viral dsRNA drives hyperinflammatory but blunted antiviral responses with enhanced PD-L1 induction in a COPD-like airway epithelial model.Biochemistry and biophysics reports · 2026Article
- Non-coding RNAs: master regulators in the battle between host antiviral defense and viral replication.Frontiers in immunology · 2026Review
- YTHDF2 Regulates Advanced Glycation End Products-Induced Melanogenesis through Inhibiting A20 Expression in Human Dermal Fibroblasts.Inflammation · 2025Article
- MicroRNAs as promising drug delivery target to ameliorate chronic obstructive pulmonary disease using nano-carriers: a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Cigarette smoke components modulate the MR1-MAIT axis.The Journal of experimental medicine · 2025Article
- Interferon and immunity: the role of microRNA in viral evasion strategies.Frontiers in immunology · 2025Review
- Identification and Experimental Validation of Biomarkers Related to MiR-125a-5p in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2025Article
- Chronic airway inflammation inFrontiers in immunology · 2025Article
- Viral strategies to antagonize the host antiviral innate immunity: an indispensable research direction for emerging virus-host interactions.Emerging microbes & infections · 2024Review
- Exploring Bioactive Phytomedicines for Advancing Pulmonary Infection Management: Insights and Future Prospects.Phytotherapy research : PTR · 2024Review
- Regulatory role of microRNAs in virus-mediated inflammation.Journal of inflammation (London, England) · 2024Review
- Review
- Generation of Myeloid-Derived Suppressor Cells Mediated by MicroRNA-125a-5p in Melanoma.International journal of molecular sciences · 2024Article
- miR-99b/let-7e/miR-125a cluster suppresses pancreatic cancer through regulation of NR6A1.American journal of cancer research · 2024Article
- MiRNAs and lncRNAs in the regulation of innate immune signaling.Non-coding RNA research · 2023Review
- Obesity dysregulates the pulmonary antiviral immune response.Nature communications · 2023Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) infections lead to severe inflammation in the airways. Patients with chronic obstructive pulmonary disease (COPD) characteristically have exaggerated airway inflammation and are more susceptible to infections with severe symptoms and increased mortality. The mechanisms that control inflammation during IAV infection and the mechanisms of immune dysregulation in COPD are unclear. We found that IAV infections lead to increased inflammatory and antiviral responses in primary bronchial epithelial cells (pBECs) from healthy nonsmoking and smoking subjects. In pBECs from COPD patients, infections resulted in exaggerated inflammatory but deficient antiviral responses. A20 is an important negative regulator of NF-κB-mediated inflammatory but not antiviral responses, and A20 expression was reduced in COPD. IAV infection increased the expression of miR-125a or -b, which directly reduced the expression of A20 and mitochondrial antiviral signaling (MAVS), and caused exaggerated inflammation and impaired antiviral responses. These events were replicated in vivo in a mouse model of experimental COPD. Thus, miR-125a or -b and A20 may be targeted therapeutically to inhibit excessive inflammatory responses and enhance antiviral immunity in IAV infections and in COPD.
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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.