ArticleCommunications biology2022
Loss of E-cadherin is causal to pathologic changes in chronic lung disease.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Therapeutic effects and potential mechanisms of astragaloside IV on pulmonary fibrosis: a systematic review and meta-analysis of preclinical studies.Frontiers in pharmacology · 2025Pooled it
- The Impact of Estrogen on Stromal Elements in the Proximal Airway in Idiopathic Subglottic Stenosis.The Laryngoscope · 2026Article
- Airway epithelial dysfunction in asthma pathogenesis: epigenetic mechanisms, inflammatory crosstalk, and therapeutic opportunities.Frontiers in allergy · 2026Review
- AFrontiers in tuberculosis · 2026Article
- Disruption of E-cadherin in the airway led to dysplastic stressed cells and asthma-like phenotypes.Developmental cell · 2025Article
- Review
- Localized Knockout of E-Cadherin in Subglottic Mucosa Increases Fibrosis.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2025Article
- Article
- Article
- Soluble E-cadherin contributes to inflammation in acute lung injury via VEGF/VEGFR2 signaling.Cell communication and signaling : CCS · 2025Article
- Role of E-cadherin in epithelial barrier dysfunction: implications for bacterial infection, inflammation, and disease pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- NLRP3 regulates epithelial barrier integrity and protects from airway hyperresponsiveness in experimental allergic asthma.Frontiers in immunology · 2025Article
- A Comprehensive Flow Cytometry Panel for Analysis of Idiopathic Subglottic Stenosis.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2024Article
- Lack of basic rationale in epithelial-mesenchymal transition and its related concepts.Cell & bioscience · 2024Review
- Microphysiological Models of Lung Epithelium-Alveolar Macrophage Co-Cultures to Study Chronic Lung Disease.Advanced biology · 2024Article
- Epigenetic Reprogramming Drives Epithelial Disruption in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2024Article
- Disinherit your Descendants by Rewriting the Chronic Pulmonary Obstructive Disease Epigenetic Script.American journal of respiratory cell and molecular biology · 2024Article
- Assessment of wood smoke induced pulmonary toxicity in normal- and chronic bronchitis-like bronchial and alveolar lung mucosa models at air-liquid interface.Respiratory research · 2024Article
- Modelling bronchial epithelial-fibroblast cross-talk in idiopathic pulmonary fibrosis (IPF) using a human-derived in vitro air liquid interface (ALI) culture.Scientific reports · 2024Article
- Dysfunctional Epithelial Barrier Is Characterized by Reduced E-Cadherin in Idiopathic Subglottic Stenosis.The Laryngoscope · 2024Article
Corrections and comments
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Authors and funding
22 authors at 1 institution in 2 countries.
Funding
Abstract
Epithelial cells line the lung mucosal surface and are the first line of defense against toxic exposures to environmental insults, and their integrity is critical to lung health. An early finding in the lung epithelium of patients with chronic obstructive pulmonary disease (COPD) is the loss of a key component of the adherens junction protein called E-cadherin. The cause of this decrease is not known and could be due to luminal insults or structural changes in the small airways. Irrespective, it is unknown whether the loss of E-cadherin is a marker or a driver of disease. Here we report that loss of E-cadherin is causal to the development of chronic lung disease. Using cell-type-specific promoters, we find that knockout of E-cadherin in alveolar epithelial type II but not type 1 cells in adult mouse models results in airspace enlargement. Furthermore, the knockout of E-cadherin in airway ciliated cells, but not club cells, increase airway hyperreactivity. We demonstrate that strategies to upregulate E-cadherin rescue monolayer integrity and serve as a potential therapeutic target.
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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.