ArticleMediators of inflammation2026
MicroRNA-223/NE Signaling Pathway Inhibits Lipopolysaccharide-Induced Acute Lung Injury by Regulating Neutrophil Extracellular Traps.
Article in Mediators of inflammation, 2026. 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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Review
- MicroRNA-223/NE Signaling Pathway Inhibits Lipopolysaccharide-Induced Acute Lung Injury by Regulating Neutrophil Extracellular Traps.Mediators of inflammation · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute lung injury (ALI) is characterized by significant neutrophil infiltration in the lungs, representing a life-threatening condition with diverse etiologies. However, the mechanisms regulating neutrophil-alveolar epithelial interactions and the pathophysiological roles of neutrophil infiltration in ALI remain incompletely understood. Methods: A dose of 20 mg/kg lipopolysaccharide (LPS) was intratracheally instilled to induce ALI models in 10-week-old male microRNA-223 knockout mice (miR-223 Results: WB experiments showed an increase in NETs-related proteins MPO and H3Cit in the lungs of WT ALI mice, with significantly enhanced expression in miR-223 Conclusion: This study reveals that the miR-223/NE axis critically regulates NETs formation, modulating neutrophil inflammatory infiltration and neutrophil-epithelial interactions to exacerbate ALI. These findings provide potential therapeutic targets for ALI.
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Registered trials
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