ReviewFrontiers in medicine2021
The Role of Hippo/YAP Signaling in Alveolar Repair and Pulmonary Fibrosis.
Review in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- [Biomechanical properties of epithelial mesenchymal transition in idiopathic pulmonary fibrosis].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2023Pooled it
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- Co-optation of the regenerative role of type 2 alveolar cells in distal lung repair in mice by terminal airway epithelial cells in humans.bioRxiv : the preprint server for biology · 2026Article
- M2 macrophage-derived extracellular vesicles (EVs) miR-155-5p promotes pulmonary fibrosis via epithelial-mesenchymal transition in lung epithelial cells.Molecular biology reports · 2026Article
- Advances in our understanding of distal progenitors in idiopathic pulmonary fibrosis: implications for novel therapeutics.The European respiratory journal · 2026Review
- Human respiratory airway progenitors derived from pluripotent cells generate alveolar epithelial cells and model pulmonary fibrosis.Nature biotechnology · 2026Article
- IPF AT2 cells are stuck in transition and biophysically dysfunctional.bioRxiv : the preprint server for biology · 2026Article
- Percolation Forces in Lung Inflammation: Determining the Path to Emphysema or Fibrosis.Biomedicines · 2026Review
- Acute Lung Injury Induced by Hyperbaric Oxygen or Other External Factors, with a Focus on Exosomes.International journal of molecular sciences · 2026Review
- Nanocarrier-Enabled siRNA Therapy for Pulmonary Fibrosis: Pharmacological Rationale, Delivery Barriers, and Translational Opportunities.International journal of nanomedicine · 2026Review
- Integrated metabolomic and transcriptomic profiling reveals lipid dysregulation and potential biomarkers in interstitial lung disease.Frontiers in immunology · 2026Article
- Multi-omic analysis reveals retinoic acid molecular drivers for dermal fibrosis and regenerative repair in the skin.Cell stem cell · 2025Article
- Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models.Nature communications · 2025Article
- Actin Branching Regulates Cell Spreading and Force on Talin, but not Activation of YAP.Cellular and molecular bioengineering · 2025Article
- Extracellular Matrix Signaling Cues: Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Fetal Tracheal Occlusion Correlates with Normalized YAP Expression and Alveolar Epithelial Differentiation in Congenital Diaphragmatic Hernia.American journal of respiratory cell and molecular biology · 2025Article
- Repairing Effect and Mechanism of the 4-Dimensionally Printed Limbal Stem Cell Strategy on Corneal Alkali Burns in Large Animals.Biomaterials research · 2025Article
- Runt-related transcription factors: from pathogenesis to therapeutic targets in multiple-organ fibrosis.Frontiers in cell and developmental biology · 2025Review
- YAP mediates HIV-related liver fibrosis.JHEP reports : innovation in hepatology · 2024Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pulmonary fibrosis is characterized by loss of normal alveoli, accumulation of pathologic activated fibroblasts, and exuberant extracellular matrix deposition that over time can lead to progressive loss of respiratory function and death. This loss of respiratory function is associated with the loss of alveolar type 1 cells (AT1) that play a crucial role in gas exchange and the depletion of the alveolar type 2 cells (AT2) that act as progenitor cells to regenerate the AT1 and AT2 cell populations during repair. Understanding the mechanisms that regulate normal alveolar repair and those associated with pathologic repair is essential to identify potential therapeutic targets to treat or delay progression of fibrotic diseases. The Hippo/YAP developmental signaling pathway has been implicated as a regulator of normal alveolar development and repair. In idiopathic pulmonary fibrosis, aberrant activation of YAP/TAZ has been demonstrated in both the alveolar epithelium and activated fibroblasts associated with increased fibrotic remodeling, and there is emerging interest in this pathway as a target for antifibrotic therapies. In this review, we summarize current evidence as to the role of the Hippo-YAP/TAZ pathway in alveolar development, homeostasis, and repair, and highlight key questions that must be resolved to determine effective strategies to modulate YAP/TAZ signaling to prevent progressive pulmonary fibrosis and enhance adaptive alveolar repair.
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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.