ArticleNature communications2024
Cell competition drives bronchiolization and pulmonary fibrosis.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed.
- ERS Congress 2025: highlights from the Basic and Translational Sciences Assembly.ERJ open research · 2026Article
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- Effects of LATS1/2 kinases inhibition on lung epithelial cells in a regeneration model.Molecular and cellular biochemistry · 2026Article
- Plasticity of Non-Apoptotic Residual Tumor Cells After Neoadjuvant Immunochemotherapy: Epigenetic and Microenvironmental Determinants.Biomolecules · 2026Review
- Extracellular matrix stiffness directs region-specific lung epithelial differentiation revealed by hPSC-derived lung organoids.Nature communications · 2026Article
- Epigenetic de-repression of basal cell metaplasia in aging AT2 cells is a risk factor for idiopathic pulmonary fibrosis (IPF).bioRxiv : the preprint server for biology · 2026Article
- Connexin 43 Loss in Endothelial Progenitors Facilitates Functional Airway Adaptation After Lung Injury.Research square · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- SYISL promotes pulmonary epithelial-mesenchymal transition and fibrosis through DSP-Hippo/YAP pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Pulmonary organoid models demonstrate compositionally driven epithelial plasticity and immune polarization.iScience · 2026Article
- TP53/TAU axis regulates microtubule bundling to control alveolar stem cell-mediated regeneration.The Journal of clinical investigation · 2026Article
- Spatial Distribution of K13-Positive Airway Epithelial Cells in Idiopathic Pulmonary Fibrosis.Biomedicines · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Review
- A ferret model demonstrates sustained fibrosis, restrictive physiology, and airway proximalization.NPJ Regenerative medicine · 2025Article
- Epithelial-mesenchymal cell competition coordinates fate transitions across tissue compartments during lung development and fibrosis.Nature communications · 2025Article
- Ferret model of bleomycin-induced lung injury shares features of human idiopathic pulmonary fibrosis.NPJ Regenerative medicine · 2025Article
- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Dysplastic lung repair fosters a tuberculosis-promoting microenvironment through maladaptive macrophage polarization.PLoS pathogens · 2025Article
- Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models.Nature communications · 2025Article
Corrections and comments
- Update of
Authors and funding
8 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive respiratory scarring disease arising from the maladaptive differentiation of lung stem cells into bronchial epithelial cells rather than into alveolar type 1 (AT1) cells, which are responsible for gas exchange. Here, we report that healthy lungs maintain their stem cells through tonic Hippo and β-catenin signaling, which promote Yap/Taz degradation and allow for low-level expression of the Wnt target gene Myc. Inactivation of upstream activators of the Hippo pathway in lung stem cells inhibits this tonic β-catenin signaling and Myc expression and promotes their Taz-mediated differentiation into AT1 cells. Vice versa, increased Myc in collaboration with Yap promotes the differentiation of lung stem cells along the basal and myoepithelial-like lineages allowing them to invade and bronchiolize the lung parenchyma in a process reminiscent of submucosal gland development. Our findings indicate that stem cells exhibiting the highest Myc levels become supercompetitors that drive remodeling, whereas loser cells with lower Myc levels terminally differentiate into AT1 cells.
Indexed as
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What Socratic 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 Socratic graph.