ArticleBiology open2025
Alveolar epithelial paxillin in postnatal lung alveolar development.
Article in Biology open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Paxillin in mechanosensitive spatial control of lung endothelial cell regeneration.NPJ Regenerative medicine · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Focal adhesion protein, paxillin plays an important role in embryonic development. We have reported that paxillin controls directional cell motility and angiogenesis. The role of paxillin in lung development remains unclear. Paxillin expression is higher in mouse pulmonary alveolar epithelial type 2 (AT2) cells at postnatal day (P)10 (alveolar stage) compared to P0 (saccular stage). The alveolar and vascular structures are disrupted, lung compliance is reduced, and the postnatal survival rate is lower in tamoxifen-induced PxniΔAT2 neonatal mice, in which the levels of paxillin in AT2 cells are knocked down. Surfactant protein expression and lamellar body structure are also inhibited in PxniΔAT2 neonatal mouse lungs. The expression of lipid transporter ABCA3 and its transcriptional regulator CEBPA that control surfactant homeostasis is inhibited in PxniΔAT2 neonatal mouse AT2 cells. These findings suggest that paxillin controls lung alveolar development through CEBPA-ABCA3 signaling in AT2 cells. Modulation of paxillin in AT2 cells may be novel interventions for neonatal lung developmental disorder.
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Registered trials
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