ArticleScientific reports2018
Characterization of a lung epithelium specific E-cadherin knock-out model: Implications for obstructive lung pathology.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05365841 (Role of Epithelial Barrier Integrity in Biologic Treatment Response of Severe Asthmatics With/Out Chronic Rhinosinusitis With Nasal Polyps), which is not on this map. Cited by 39 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
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.
Role of Epithelial Barrier Integrity in Biologic Treatment Response of Severe Asthmatics With/Out Chronic Rhinosinusitis With Nasal Polyps (CRSwNP). Can Shedding of Epithelial Barrier Proteins be Used as Biomarker in Severe Asthma With/Out CRSwNP Management?
Who cites it
39 citing papers in PubMed, 70 citations in OpenAlex.
- The role of alveolar epithelial junctions in early lung injury and COVID-19-induced fibrosis.Histochemistry and cell biology · 2026Article
- Targeting Tight Junction Proteins to Restore Airway Epithelial Barrier Function in Asthma.Current allergy and asthma reports · 2026Review
- An Ex Vivo Model of Post Infectious Bronchiolitis Obliterans in Children Using Reconstituted Human Bronchial Epithelium.Biomolecules · 2026Article
- Integrated airway epithelial signaling networks linking allergen-driven inflammation to airway remodeling in asthma.Frontiers in immunology · 2026Review
- Airway epithelial dysfunction in asthma pathogenesis: epigenetic mechanisms, inflammatory crosstalk, and therapeutic opportunities.Frontiers in allergy · 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
- Next Decade Research in Asthma: Broad Omics-Based Exploration Versus Targeted Airway Epithelium Studies.Journal of clinical medicine · 2025Review
- Disruption of E-cadherin in the airway led to dysplastic stressed cells and asthma-like phenotypes.Developmental cell · 2025Article
- Unflavored electronic cigarette exposure induces alterations in airway ciliary structure and function.Respiratory research · 2025Article
- Soluble E-cadherin contributes to inflammation in acute lung injury via VEGF/VEGFR2 signaling.Cell communication and signaling : CCS · 2025Article
- Generation of Human 3D Airway Assembloids for Advanced Modeling.International journal of biological sciences · 2025Article
- NLRP3 regulates epithelial barrier integrity and protects from airway hyperresponsiveness in experimental allergic asthma.Frontiers in immunology · 2025Article
- TRPV4 Mediates Alveolar Epithelial Barrier Integrity and Induces ADAM10-Driven E-Cadherin Shedding.Cells · 2024Article
- The epithelial era of asthma research: knowledge gaps and future direction for patient care.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Fungal Aeroallergens-The Impact of Climate Change.Journal of fungi (Basel, Switzerland) · 2023Review
- Tight Junctions, the Epithelial Barrier, and Toll-like Receptor-4 During Lung Injury.Inflammation · 2022Review
- Loss of E-cadherin is causal to pathologic changes in chronic lung disease.Communications biology · 2022Article
- Epithelial coxsackievirus adenovirus receptor promotes house dust mite-induced lung inflammation.Nature communications · 2022Article
- The relation between age and airway epithelial barrier function.Respiratory research · 2022Article
- Fundamentals of vaping-associated pulmonary injury leading to severe respiratory distress.Life science alliance · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
The airway epithelium regulates responses to aeroallergens, acting as a physical and immunological barrier. In asthma, epithelial barrier function and the expression of adherens junction protein E-cadherin is compromised, but it is unknown whether this is cause or consequence of the disease. We hypothesized that airway epithelial loss of E-cadherin is a critical step in the development of manifestations of asthma. We generated a transgenic mouse model with conditional loss of E-cadherin in lung epithelial cells at birth and onwards. We observed normal lung development at the time of birth in mice lacking E-cadherin in the lung epithelium. However, E-cadherin deficiency led to progressive epithelial damage in mice growing into adulthood, as evidenced by airway epithelial denudation, decreased zonula occludens (ZO)-1 expression, loss of ciliated cells, and enlarged alveolar spaces. In addition, spontaneous goblet cell metaplasia with mucus production was observed. These epithelial changes were accompanied by elevated levels of the epithelial-derived chemokine CCL17, infiltration of eosinophils and dendritic cells, and mucus production. In conclusion, loss of E-cadherin induces features in the lung reminiscent of those observed in asthma, indicating that the disruption of E-cadherin-mediated cell-cell contacts may play a key role in the development of asthma manifestations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.