ArticleDevelopmental cell2025
Disruption of E-cadherin in the airway led to dysplastic stressed cells and asthma-like phenotypes.
Article in Developmental cell, 2025. 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.
- Targeting Tight Junction Proteins to Restore Airway Epithelial Barrier Function in Asthma.Current allergy and asthma reports · 2026Review
- CC16 alleviates PM2.5-induced airway inflammation in asthmatic mice by targeting the E-cadherin-mediated ferroptosis regulatory axis.Current research in toxicology · 2026Article
- Airway epithelial dysfunction in asthma pathogenesis: epigenetic mechanisms, inflammatory crosstalk, and therapeutic opportunities.Frontiers in allergy · 2026Review
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Authors and funding
15 authors.
Funding
Abstract
While E-cadherin is a known core component of the adherens junction, how it controls cell fate remains poorly understood. Here, we show that in the mouse airway, inactivation of E-cadherin in epithelial progenitor club cells, but not terminally differentiated ciliated cells, led to increased proliferation, goblet cell metaplasia, and immune infiltration, mimicking asthma phenotypes without exposure to allergen. Single-cell RNA sequencing identified a cellular stress signature in the mutant airway; a profile previously associated with dysplastic alveolar transitional cells in fibrotic lungs. Chemokine genes such as Cxcl17 are upregulated in the mutant airway both in vivo and when cultured in isolation, identifying an intrinsic ability of the epithelium to sense junction breach and launch immune defense. Inactivation of Il4ra in the mutant attenuated goblet cell metaplasia, but not immune recruitment. Together, these findings demonstrate that loss of E-cadherin leads to airway remodeling through both an epithelium-intrinsic mechanism and epithelium-immune crosstalk.
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Registered trials
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