ArticleJCI insight2019
TAZ is required for lung alveolar epithelial cell differentiation after injury.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 91 citations in OpenAlex.
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- Efficient genome editing in ASC-derived porcine lung organoids via GFP-guided enrichment.Stem cell research & therapy · 2026Article
- Advances in our understanding of distal progenitors in idiopathic pulmonary fibrosis: implications for novel therapeutics.The European respiratory journal · 2026Review
- A diagnostic model based on pulmonary microbiota and host gene expression to distinguish colonization from pneumonia.Scientific reports · 2026Article
- Metabolic permissiveness: how tissue context shapes cancer.Genes & development · 2026Review
- Human respiratory airway progenitors derived from pluripotent cells generate alveolar epithelial cells and model pulmonary fibrosis.Nature biotechnology · 2026Article
- Review
- Transcriptomic signature-guided depletion of intermediate alveolar epithelial cells ameliorates pulmonary fibrosis in mice.Nature communications · 2026Article
- Mechanosensing Pathways in the Progression of Pulmonary Fibrosis.Current opinion in biomedical engineering · 2025Article
- Mechanotransduction: A Master Regulator of Alveolar Cell Fate Determination.Bioengineering (Basel, Switzerland) · 2025Review
- ITIH4 attenuates acute lung injury by Fe-containing particulate matter in mice via Hippo pathway in type II alveolar epithelial cells.Respiratory research · 2025Article
- Lung organoids in COPD: recent advances and future prospects.Respiratory research · 2025Review
- PCLAF-DREAM drives alveolar cell plasticity for lung regeneration.Nature communications · 2024Article
- Influence of intersignaling crosstalk on the intracellular localization of YAP/TAZ in lung cells.Cell communication and signaling : CCS · 2024Review
- Generation of human alveolar epithelial type I cells from pluripotent stem cells.Cell stem cell · 2024Article
- Advances and Applications of Lung Organoids in the Research on Acute Respiratory Distress Syndrome (ARDS).Journal of clinical medicine · 2024Review
- TAZ deficiency impairs the autophagy-lysosomal pathway through NRF2 dysregulation and lysosomal dysfunction.International journal of biological sciences · 2024Article
- Role of DCLK1/Hippo pathway in type II alveolar epithelial cells differentiation in acute respiratory distress syndrome.Molecular medicine (Cambridge, Mass.) · 2023Article
- Epithelial Yap/Taz are required for functional alveolar regeneration following acute lung injury.JCI insight · 2023Article
- Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lung is a relatively quiescent organ during homeostasis, but has a remarkable capacity for repair after injury. Alveolar epithelial type I cells (AEC1s) line airspaces and mediate gas exchange. After injury, they are regenerated by differentiation from their progenitors - alveolar epithelial type II cells (AEC2s) - which also secrete surfactant to maintain surface tension and alveolar patency. While recent studies showed that the maintenance of AEC2 stemness is Wnt dependent, the molecular mechanisms underlying AEC2-AEC1 differentiation in adult lung repair are still incompletely understood. Here we show that WWTR1 (TAZ) plays a crucial role in AEC differentiation. Using an in vitro organoid culture system, we found that tankyrase inhibition can efficiently block AEC2-AEC1 differentiation, and this effect was due to the inhibition of TAZ. In a bleomycin induced lung injury model, conditional deletion of TAZ in AEC2s dramatically reduced AEC1 regeneration during recovery, leading to exacerbated alveolar lesions and fibrosis. In patients with idiopathic pulmonary fibrosis (IPF), decreased blood levels of RAGE, a biomarker of AEC1 health, were associated with more rapid disease progression. Our findings implicate TAZ as a critical factor involved in AEC2 to AEC1 differentiation, and hence the maintenance of alveolar integrity after injury.
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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.