ArticleCell death & disease2017
Ly6G+ neutrophil-derived miR-223 inhibits the NLRP3 inflammasome in mitochondrial DAMP-induced acute lung injury.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 100 citations in OpenAlex.
- Neuroimmune Regulation of NLRP3 Signalling in Parkinson's Disease.Molecular neurobiology · 2026Review
- Mitochondria as convergence hubs for innate immunity pathways.Communications biology · 2026Review
- miRNAs-neutrophil axis: novel insights into acute lung injury and chronic inflammatory lung diseases.Frontiers in immunology · 2026Review
- Circulating microRNAs and Plasma Gelsolin as Biomarkers of Sepsis: Molecular Insights and Prospects for Precision Medicine.Biomolecules · 2025Review
- NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025Review
- Article
- Yunvjian decoction attenuates lipopolysaccharide-induced acute lung injury by inhibiting NF-κB/NLRP3 pathway and pyroptosis.Frontiers in pharmacology · 2025Article
- Roles of microRNAs in acute lung injury and acute respiratory distress syndrome: mechanisms and clinical potential.Frontiers in immunology · 2025Review
- The Central Role of Interleukin-1 Signalling in the Pathogenesis of Kawasaki Disease Vasculitis: Path to Translation.The Canadian journal of cardiology · 2024Review
- MiR-223-3p in Cancer Development and Cancer Drug Resistance: Same Coin, Different Faces.International journal of molecular sciences · 2024Review
- Macrophage biomimetic nanoparticle-targeted functional extracellular vesicle micro-RNAs revealed via multiomics analysis alleviate sepsis-induced acute lung injury.Journal of nanobiotechnology · 2024Article
- IL-18 biology in severe asthma.Frontiers in medicine · 2024Review
- Inflammasomes cross-talk with lymphocytes to connect the innate and adaptive immune response.Journal of advanced research · 2023Review
- Extracellular vesicle-transmitted miR-671-5p alleviates lung inflammation and injury by regulating the AAK1/NF-κB axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- The ultimate tradeoff: how red cell adaptations to malaria alter the host response during critical illness.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Sex-biased expression of selected chromosome x-linked microRNAs with potent regulatory effect on the inflammatory response in children with cystic fibrosis: A preliminary pilot investigation.Frontiers in immunology · 2023Article
- miR-223: a key regulator of pulmonary inflammation.Frontiers in medicine · 2023Review
- Review
- Mitochondrial citrate accumulation drives alveolar epithelial cell necroptosis in lipopolysaccharide-induced acute lung injury.Experimental & molecular medicine · 2022Article
- Sex difference in innate inflammatory response and macrophage polarization in Streptococcus agalactiae-induced pneumonia and potential role of microRNA-223-3p.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miRNA) mediates RNA interference to regulate a variety of innate immune processes, but how miRNAs coordinate the mechanisms underlying acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in patients with pulmonary inflammatory injury is still unknown. In this study, we demonstrated that miR-223 limits the number of Ly6G+ neutrophils and inhibits the activity of the NLRP3 inflammasome to alleviate ALI induced by mitochondrial damage-associated molecular patterns (DAMPs) (MTDs). miR-223 expression is increased in the lungs of MTD-induced mice or ARDS patients following trauma/transfusion or following the physiological remission of ALI/ARDS. miR-223-/+ mice exhibited more severe ALI and cytokine dysregulation. Other studies have shown that MTD-induced increases in miR-223 expression are mainly contributed by Ly6G+ neutrophils from the haematopoietic system. miR-223 blocks bone marrow-derived Ly6G+ neutrophil differentiation and inhibits peripheral cytokine release. In addition, MTD-induced miR-223 expression activates a negative feedback pathway that targets the inhibition of NLRP3 expression and IL-1β release; therefore, miR-223 deficiency can lead to the sustained activation of NLRP3-IL-1β. Finally, elimination of peripheral Ly6G+ neutrophils and pharmacological blockade of the miR-223-NLRP3-IL-1β signalling axis could alleviate MTD-induced ALI. In summary, miR-223 is essential for regulating the pathogenesis of DAMP-induced ALI.
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