ArticleCell death discovery2020
IL-33-induced neutrophil extracellular traps degrade fibronectin in a murine model of bronchopulmonary dysplasia.
Article in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- Macrophage-derived fibronectin suppresses antitumor immunity via tissue stiffening and immunosuppressive cell induction in cancer mouse models.Nature communications · 2026Article
- Caffeine inhibited the hyperoxia-induced A2AR-ERK/p38 MAPK-IL-8 pathway in type II alveolar epithelial cells to suppress NETs formation in bronchopulmonary dysplasia.Pediatric research · 2026Article
- CCL5 deficiency aggravates acute DSS-induced colitis by restricting IL-33-induced formation of Tregs in intestinal tract.Clinical science (London, England : 1979) · 2026Article
- Role of connexin 43 in hyperoxia-induced bronchopulmonary dysplasia and associated pulmonary hypertension.PloS one · 2026Article
- The Ly6gCancer communications (London, England) · 2026Article
- MiR-203a-3p in extracellular vesicles derived from mesenchymal stem cells alleviates BPD-associated apoptosis and inflammation.Stem cell research & therapy · 2025Article
- GPRC5A/CXCL8/NLRP3-mediated neutrophil extracellular traps drive gemcitabine-nab-paclitaxel resistance in pancreatic adenocarcinoma.Cancer biology & medicine · 2025Article
- The Destructive Cycle in Bronchopulmonary Dysplasia: The Rationale for Systems Pharmacology Therapeutics.Antioxidants (Basel, Switzerland) · 2025Review
- Exploring neutrophil extracellular traps: mechanisms of immune regulation and future therapeutic potential.Experimental hematology & oncology · 2025Review
- Lenvatinib-activated NDUFA4L2/IL33/PADI4 pathway induces neutrophil extracellular traps that inhibit cuproptosis in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Machine Learning Identification of Neutrophil Extracellular Trap-Related Genes as Potential Biomarkers and Therapeutic Targets for Bronchopulmonary Dysplasia.International journal of molecular sciences · 2025Article
- Thrombospondin-1 Airway Expression and Thrombospondin-1 Gene Variants Are Associated with Bronchopulmonary Dysplasia in Extremely Low-Birth-Weight Infants: A Pilot Study.Children (Basel, Switzerland) · 2025Article
- IL-33, a neutrophil extracellular trap-related gene involved in the progression of diabetic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Macrophage pyroptosis mediates hyperoxia-induced inflammatory lung injury in neonates.Frontiers in immunology · 2025Article
- Fetal origin of bronchopulmonary dysplasia: contribution of intrauterine inflammation.Molecular medicine (Cambridge, Mass.) · 2024Review
- Recruitment of PVT1 Enhances YTHDC1-Mediated m6A Modification of IL-33 in Hyperoxia-Induced Lung Injury During Bronchopulmonary Dysplasia.Inflammation · 2024Article
- Tenascin-C modulates alveolarization in bronchopulmonary dysplasia.Inflammation and regeneration · 2024Article
- Disrupted TGF-β signaling: a link between bronchopulmonary dysplasia and alveolar type 1 cells.The Journal of clinical investigation · 2024Article
- SLE serum induces altered goblet cell differentiation and leakiness in human intestinal organoids.EMBO molecular medicine · 2024Article
- New targets for type 2-low asthma.The Korean journal of internal medicine · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bronchopulmonary dysplasia (BPD) is the leading cause of chronic lung disease in preterm neonates. Extracellular matrix (ECM) abnormalities reshape lung development, contributing to BPD progression. In the present study, we first discovered that the ECM component fibronectin was reduced in the pulmonary tissues of model mice with BPD induced by lipopolysaccharide (LPS) and hyper-oxygen. Meanwhile, interleukin-33 (IL-33) and other inflammatory cytokines were elevated in BPD lung tissues. LPS stimulated the production of IL-33 in alveolar epithelial cells via myeloid differentiation factor 88 (MyD88), protein 38 (p38), and nuclear factor-kappa B (NF-κB) protein 65 (p65). Following the knockout of either IL-33 or its receptor suppression of tumorigenicity 2 (ST2) in mice, BPD disease severity was improved, accompanied by elevated fibronectin. ST2 neutralization antibody also relieved BPD progression and restored the expression of fibronectin. IL-33 induced the formation of neutrophil extracellular traps (NETs), which degraded fibronectin in alveolar epithelial cells. Moreover, DNase-mediated degradation of NETs was protective against BPD. Finally, a fibronectin inhibitor directly decreased fibronectin and caused BPD-like disease in the mouse model. Our findings may shed light on the roles of IL-33-induced NETs and reduced fibronectin in the pathogenesis of BPD.
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