ArticleEuropean journal of medical research2025
The miR-3164/PAD4 axis regulates NETosis to prevent airway inflammation and remodeling through the TLR2/NF-κB signaling pathway.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- MicroRNAs-Are They Possible Markers of Allergic Diseases and Efficient Immunotherapy?International journal of molecular sciences · 2026Review
- Predicting Multidrug-Resistant Pneumonia: An Interpretable Machine Learning Model Validated in US and Chinese Patient Cohorts.Infection and drug resistance · 2026Article
- miRNAs-neutrophil axis: novel insights into acute lung injury and chronic inflammatory lung diseases.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlleviating airway inflammation and reversing airway remodeling are critical therapeutic objectives in asthma treatment. This study aimed to investigate the role of miR-3164 in regulating PAD4-mediated NETosis and to elucidate the underlying mechanisms through which it attenuates airway inflammation and reverses remodeling.
methodsThe effects of miR-3164 on PAD4 expression and neutrophil extracellular trap (NET) formation were evaluated via dual-luciferase reporter assays, Western blotting, quantitative real-time PCR (qRT‒PCR), and flow cytometry. The influence of neutrophils treated with miR-3164 mimics on the proliferation and migration of mouse airway smooth muscle cells (ASMCs) was assessed via MTT and Transwell assays.
resultsThe dual-luciferase reporter assay confirmed a targeting relationship between miR-3164 and PAD4. Treatment with miR-3164 mimics suppressed PAD4 expression in neutrophils and significantly altered the levels of myeloperoxidase (MPO) and neutrophil elastase (NE) within NETs. These effects confer the ability of miR-3164 mimics to markedly downregulate the expression of inflammation- and airway remodeling-related biomarkers, including TLR2, IκBα, NF-κB, calponin, α-SMA, and E-cadherin, in airway smooth muscle cells (ASMCs). Furthermore, NETs treated with miR-3164 mimics significantly attenuated the viability and migration capacity of ASMCs exposed to LPS and ATP.
conclusionsOur findings demonstrate that modulating NETosis represents a potential therapeutic strategy to attenuate airway inflammatory responses and remodeling via the TLR2/NF-κB signaling pathway, thereby offering a novel target for the treatment of asthma. CLINICAL TRIAL NUMBER: Not applicable.
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