ArticleThe European respiratory journal2025
Targeting IL6-Edn1-FoxO1 axis enables lung growth in mechanically ventilated newborn mice.
Article in The European respiratory journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Mechanisms and clinical research progress of IL-6-mediated crosstalk between the alveolar microenvironment and the immune system in patients with severe pneumonia undergoing mechanical ventilation.Frontiers in immunology · 2026Review
- Revisiting ventilator-induced lung injury: from mechanical power to immunometabolic interaction.Frontiers in immunology · 2026Review
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24 authors.
Funding
Abstract
rationaleMechanical ventilation is a life-saving treatment for preterm infants that often leads to bronchopulmonary dysplasia (BPD). We previously demonstrated a reduced number of alveolar epithelial cells with a depletion of alveolar epithelial type 2 cells (AT2) in lungs of infants with BPD.
objectiveTo investigate and target the mechanisms by which mechanical ventilation causes an arrest of alveolarisation.
methodsExperimental mouse model of neonatal ventilation-induced lung injury (VILI) in wild-type mice,
resultsMechanical ventilation leads to an AT2 depletion and arrest of alveolar growth. Transcriptomic profiling, measurement of gene and protein expression, immunofluorescent staining as well as cell culture studies identified an IL-6-mediated expression of Endothelin-1 (Edn1) and a nuclear sequestration of the antiproliferative transcription factor FoxO1 in AT2. These findings were confirmed using murine PCLS, lung epithelial cells and transgenic mice with inducible constitutive active FoxO1.
conclusionMechanical ventilation causes an arrest of alveolarisation in newborn mice through an IL-6-mediated activation of Edn1 signalling and nuclear sequestration of FoxO1 in AT2. Thus, this study provides rationale for considering pharmacological inhibition of IL-6 and/or endothelin receptors as a therapeutic strategy for preterm newborns at risk of VILI-associated lung growth arrest.
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