ArticleThe EMBO journal2022
Airway secretory cell fate conversion via YAP-mTORC1-dependent essential amino acid metabolism.
Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- Transitional cell states at the crossroads of development, disease, and repair-regeneration.Physiological reviews · 2026Review
- Pulmonary organoid models demonstrate compositionally driven epithelial plasticity and immune polarization.iScience · 2026Article
- Refractory Lung Diseases: From Cellular Structures, Molecular Mechanisms to Therapeutic Strategies.Pediatric discovery · 2026Review
- Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models.Nature communications · 2025Article
- Case report: refractory atelectasis after infection of adenovirus and Mycoplasma Pneumoniae in an immunocompetent patient.BMC pulmonary medicine · 2025Article
- Safely Targeting Cancer, the Wound That Never Heals, Utilizing CBP/Beta-Catenin Antagonists.Cancers · 2025Article
- Linking signaling dynamics and cell fate decisions through single-cell imaging: evidence and challenges.Frontiers in cell and developmental biology · 2025Review
- Carbon chain elongation microorganism stimulates caproate production from ethanol and acetate under applied voltage regulation.Frontiers in microbiology · 2025Article
- Identifying the Role of YAP in the Development of Rumen Epithelium Using 3D Organoid.Stem cells international · 2025Article
- Cell competition drives bronchiolization and pulmonary fibrosis.Nature communications · 2024Article
- IFN-γ and YAP lead epithelial cells astray after severe respiratory infection.The Journal of clinical investigation · 2024Article
- Influence of intersignaling crosstalk on the intracellular localization of YAP/TAZ in lung cells.Cell communication and signaling : CCS · 2024Review
- YAP/TAZ: Molecular pathway and disease therapy.MedComm · 2023Review
- Potential Roles of YAP/TAZ Mechanotransduction in Spaceflight-Induced Liver Dysfunction.International journal of molecular sciences · 2023Review
- TRIB3 Mediates Fibroblast Activation and Fibrosis though Interaction with ATF4 in IPF.International journal of molecular sciences · 2022Article
- Airway secretory cell fate conversion via YAP-mTORC1-dependent essential amino acid metabolism.The EMBO journal · 2022Article
- Functional and clinical characteristics of focal adhesion kinases in cancer progression.Frontiers in cell and developmental biology · 2022Review
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 3 institutions in 3 countries.
Funding
Abstract
Tissue homeostasis requires lineage fidelity of stem cells. Dysregulation of cell fate specification and differentiation leads to various diseases, yet the cellular and molecular mechanisms governing these processes remain elusive. We demonstrate that YAP/TAZ activation reprograms airway secretory cells, which subsequently lose their cellular identity and acquire squamous alveolar type 1 (AT1) fate in the lung. This cell fate conversion is mediated via distinctive transitional cell states of damage-associated transient progenitors (DATPs), recently shown to emerge during injury repair in mouse and human lungs. We further describe a YAP/TAZ signaling cascade to be integral for the fate conversion of secretory cells into AT1 fate, by modulating mTORC1/ATF4-mediated amino acid metabolism in vivo. Importantly, we observed aberrant activation of the YAP/TAZ-mTORC1-ATF4 axis in the altered airway epithelium of bronchiolitis obliterans syndrome, including substantial emergence of DATPs and AT1 cells with severe pulmonary fibrosis. Genetic and pharmacologic inhibition of mTORC1 activity suppresses lineage alteration and subepithelial fibrosis driven by YAP/TAZ activation, proposing a potential therapeutic target for human fibrotic lung diseases.
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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.