ArticleThe Journal of clinical investigation2006
Blocking airway mucous cell metaplasia by inhibiting EGFR antiapoptosis and IL-13 transdifferentiation signals.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
156 citing papers in PubMed, 1 synthesis or guideline pooled it, 259 citations in OpenAlex.
- Management of airway mucus hypersecretion in chronic airway inflammatory disease: Chinese expert consensus (English edition).International journal of chronic obstructive pulmonary disease · 2018Guideline
- CD45/CD11b positive subsets of adult lung anchorage-independent cells harness epithelial stem cells in culture.Journal of tissue engineering and regenerative medicine · 2013Trial
- Macrophage pyroptosis drives luminal senescence and club-cell reprogramming in 5α-reductase inhibitor-treated prostatic hyperplasia.Experimental & molecular medicine · 2026Article
- Structural and cellular mechanisms of mucus plugging in the larger airways.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Airway Goblet Metaplasia Resulting from YAP/TAZ Deletion Drives Pulmonary Inflammatory Responses.American journal of respiratory cell and molecular biology · 2026Article
- Integrated airway epithelial signaling networks linking allergen-driven inflammation to airway remodeling in asthma.Frontiers in immunology · 2026Review
- Transcriptional coordination in multicellular lineage differentiation during lung organogenesis: deciphering the role of epithelial cells as a microenvironmental regulatory hub.Frontiers in cell and developmental biology · 2026Review
- Extracellular vesicle-based delivery to airway basal cells for durable gene therapy in cystic fibrosis.Frontiers in bioengineering and biotechnology · 2026Review
- Article
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- The long reach of influenza and other respiratory viruses: from acute epithelial injury to post-viral lung disease.Clinical microbiology reviews · 2025Review
- Undocking of an extensive ciliary network induces proteostasis and cell fate switching resulting in severe primary ciliary dyskinesia.Science translational medicine · 2025Article
- Airway epithelial cell-specific deletion of EGFR modulates mucoinflammatory features of cystic fibrosis-like lung disease in mice.Frontiers in immunology · 2025Article
- Novel insights into the study of goblet cell hypersecretion in allergic rhinitis.Frontiers in immunology · 2025Review
- Potential applications and mechanisms of natural products in mucosal-related diseases.Frontiers in immunology · 2025Review
- Hippo cooperates with p53 to regulate lung airway mucous cell metaplasia.Disease models & mechanisms · 2024Article
- MAPK13 controls structural remodeling and disease after epithelial injury.bioRxiv : the preprint server for biology · 2024Article
- A correctable immune niche for epithelial stem cell reprogramming and post-viral lung diseases.The Journal of clinical investigation · 2024Article
- Anti-Inflammatory and Anti-Oxidant Properties of N-Acetylcysteine: A Fresh Perspective.Journal of clinical medicine · 2024Review
- Loss of an extensive ciliary connectome induces proteostasis and cell fate switching in a severe motile ciliopathy.bioRxiv : the preprint server for biology · 2024Article
96 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial hyperplasia and metaplasia are common features of inflammatory and neoplastic disease, but the basis for the altered epithelial phenotype is often uncertain. Here we show that long-term ciliated cell hyperplasia coincides with mucous (goblet) cell metaplasia after respiratory viral clearance in mouse airways. This chronic switch in epithelial behavior exhibits genetic susceptibility and depends on persistent activation of EGFR signaling to PI3K that prevents apoptosis of ciliated cells and on IL-13 signaling that promotes transdifferentiation of ciliated to goblet cells. Thus, EGFR blockade (using an irreversible EGFR kinase inhibitor designated EKB-569) prevents virus-induced increases in ciliated and goblet cells whereas IL-13 blockade (using s-IL-13Ralpha2-Fc) exacerbates ciliated cell hyperplasia but still inhibits goblet cell metaplasia. The distinct effects of EGFR and IL-13 inhibitors after viral reprogramming suggest that these combined therapeutic strategies may also correct epithelial architecture in the setting of airway inflammatory disorders characterized by a similar pattern of chronic EGFR activation, IL-13 expression, and ciliated-to-goblet cell metaplasia.
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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.