ArticleNPJ Regenerative medicine2024
Airway epithelial cell identity and plasticity are constrained by Sox2 during lung homeostasis, tissue regeneration, and in human disease.
Article in NPJ Regenerative medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 11 citations in OpenAlex.
- Concurrent jamming and mesenchymal-to-epithelial transitions during airway basal stem cell differentiation.iScience · 2026Article
- Bioinformatics-driven genome-wide identification of viral miRNAs in high spillover bat coronaviruses and their target genes in human.Archives of microbiology · 2026Article
- Dysplastic Epithelial Repair Propagates Chronic Pathology Through the Paracrine Transformation of Pulmonary Fibroblasts.bioRxiv : the preprint server for biology · 2026Article
- Spatial Distribution of K13-Positive Airway Epithelial Cells in Idiopathic Pulmonary Fibrosis.Biomedicines · 2026Article
- Characterization of subchronic lung and brain consequences caused by mouse-adapted SARS-CoV-2 and influenza A infection of C57BL6 mice.Frontiers in immunology · 2026Article
- Examining the role of Notch signaling in dysplastic lung repair.BMC research notes · 2025Article
- Article
- Cellular senescence-related gene signatures in idiopathic pulmonary fibrosis: insights from bioinformatics.Frontiers in immunology · 2025Article
- Impact of particulate air pollution on airway injury and epithelial plasticity; underlying mechanisms.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Maintenance of the cellular boundary between airway and alveolar compartments during homeostasis and after injury is essential to prohibit pathological plasticity which can reduce respiratory function. Lung injury and disease can induce either functional alveolar epithelial regeneration or dysplastic formation of keratinized epithelium which does not efficiently contribute to gas exchange. Here we show that Sox2 preserves airway cell identity and prevents fate changes into either functional alveolar tissue or pathological keratinization following lung injury. Loss of Sox2 in airway epithelium leads to a loss of airway epithelial identity with a commensurate gain in alveolar and basal cell identity, in part due to activation of Wnt signaling in secretory cells and increased Trp63 expression in intrapulmonary basal-like progenitors. In idiopathic pulmonary fibrosis, loss of SOX2 expression correlates with increased WNT signaling activity in dysplastic keratinized epithelium. SOX2-deficient dysplastic epithelial cells are also observed in COVID-19 damaged lungs. Thus, Sox2 provides a molecular barrier that suppresses airway epithelial plasticity to prevent acquisition of alveolar or basal cell identity after injury and help guide proper epithelial fate and regeneration.
Identifiers
What OpenQuestion holds
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.