ArticleJCI insight2018
Active epithelial Hippo signaling in idiopathic pulmonary fibrosis.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
92 citing papers in PubMed, 147 citations in OpenAlex.
- Sirolimus suppresses circulating fibrocytes in idiopathic pulmonary fibrosis in a randomized controlled crossover trial.JCI insight · 2023Trial
- Review
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- Nanoparticle-mediated inhibition of Yes-associated protein prevents corneal scarring after traumatic injury.Materials today. Bio · 2026Article
- YAP as a therapeutic target in esophageal squamous cell carcinoma: insights and strategies.Annals of medicine · 2025Review
- Epithelial damage and ageing: the perfect storm.Thorax · 2025Review
- Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models.Nature communications · 2025Article
- Uncovering an antifibrotic Prrx1-lineage mesenchymal cell subpopulation in fibrotic lungs.Disease models & mechanisms · 2025Article
- Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Review
- YAP as a potential therapeutic target for myofibroblast formation in asthma.Respiratory research · 2025Article
- Spindle localization of YAP/TAZ maintains even distribution of YAP/TAZ in daughter cells.Journal of biosciences · 2025Article
- Cell competition drives bronchiolization and pulmonary fibrosis.Nature communications · 2024Article
- Inhibiting endothelial cell Mst1 attenuates acute lung injury in mice.JCI insight · 2024Article
- Review
- Genetics and Genomics of Pulmonary Fibrosis: Charting the Molecular Landscape and Shaping Precision Medicine.American journal of respiratory and critical care medicine · 2024Review
- Biomechanical Properties and Cellular Responses in Pulmonary Fibrosis.Bioengineering (Basel, Switzerland) · 2024Review
- Targeting the Hippo pathway to prevent radioresistance brain metastases from the lung (Review).International journal of oncology · 2024Review
- Mechanotransduction-induced interplay between phospholamban and yes-activated protein induces smooth muscle cell hypertrophy.Mucosal immunology · 2024Article
- Influence of intersignaling crosstalk on the intracellular localization of YAP/TAZ in lung cells.Cell communication and signaling : CCS · 2024Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Hippo/YAP signaling plays pleiotropic roles in the regulation of cell proliferation and differentiation during organogenesis and tissue repair. Herein we demonstrate increased YAP activity in respiratory epithelial cells in lungs of patients with idiopathic pulmonary fibrosis (IPF), a common, lethal form of interstitial lung disease (ILD). Immunofluorescence staining in IPF epithelial cells demonstrated increased nuclear YAP and loss of MST1/2. Bioinformatic analyses of epithelial cell RNA profiles predicted increased activity of YAP and increased canonical mTOR/PI3K/AKT signaling in IPF. Phospho-S6 (p-S6) and p-PTEN were increased in IPF epithelial cells, consistent with activation of mTOR signaling. Expression of YAP (S127A), a constitutively active form of YAP, in human bronchial epithelial cells (HBEC3s) increased p-S6 and p-PI3K, cell proliferation and migration, processes that were inhibited by the YAP-TEAD inhibitor verteporfin. Activation of p-S6 was required for enhancing and stabilizing YAP, and the p-S6 inhibitor temsirolimus blocked nuclear YAP localization and suppressed expression of YAP target genes CTGF, AXL, and AJUBA (JUB). YAP and mTOR/p-S6 signaling pathways interact to induce cell proliferation and migration, and inhibit epithelial cell differentiation that may contribute to the pathogenesis of IPF.
Indexed as
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.