ArticleAmerican journal of respiratory cell and molecular biology2019
Nascent Lung Organoids Reveal Epithelium- and Bone Morphogenetic Protein-mediated Suppression of Fibroblast Activation.
Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026Review
- Bidirectional fibrogenic cross-talk revealed in a human iPSC-derived epithelial-mesenchymal co-culture model of pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Human lung organoids model for assessing host response toFrontiers in cellular and infection microbiology · 2026Article
- A Unified Map of Airway Interactions: Secretome and Mechanotransduction Loops from Development to Disease.Advances in respiratory medicine · 2025Review
- Targeting CEBPA to restore cellular identity and tissue homeostasis in pulmonary fibrosis.JCI insight · 2024Article
- RNA-sequencing reveals differential fibroblast responses to bleomycin and pneumonectomy.Physiological reports · 2024Article
- Realveolarization with inhalable mucus-penetrating lipid nanoparticles for the treatment of pulmonary fibrosis in mice.Science advances · 2024Article
- The evolution ofEuropean respiratory review : an official journal of the European Respiratory Society · 2024Review
- Autologous Airway Basal Cell Transplantation Alleviates Airway Epithelium Defect in Recurrent Benign Tracheal Stenosis.Stem cells translational medicine · 2023Article
- Chemical Modification of Human Decellularized Extracellular Matrix for Incorporation into Phototunable Hybrid-Hydrogel Models of Tissue Fibrosis.ACS applied materials & interfaces · 2023Article
- NF-κB drives epithelial-mesenchymal mechanisms of lung fibrosis in a translational lung cell model.JCI insight · 2023Article
- Engineering and Modeling the Lung Mesenchyme.Advances in experimental medicine and biology · 2023Article
- Engineering Dynamic 3D Models of Lung.Advances in experimental medicine and biology · 2023Article
- Alveolar epithelial cells and microenvironmental stiffness synergistically drive fibroblast activation in three-dimensional hydrogel lung models.Biomaterials science · 2022Article
- Bone morphogenetic protein 4 inhibits pulmonary fibrosis by modulating cellular senescence and mitophagy in lung fibroblasts.The European respiratory journal · 2022Article
- Harnessing conserved signaling and metabolic pathways to enhance the maturation of functional engineered tissues.NPJ Regenerative medicine · 2022Review
- Mouse lung organoid responses to reduced, increased, and cyclic stretch.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Open questions in human lung organoid research.Frontiers in pharmacology · 2022Review
- Disease modeling of pulmonary fibrosis using human pluripotent stem cell-derived alveolar organoids.Stem cell reports · 2021Article
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9 authors at 1 institution in 1 country.
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Abstract
Reciprocal epithelial-mesenchymal interactions are pivotal in lung development, homeostasis, injury, and repair. Organoids have been used to investigate such interactions, but with a major focus on epithelial responses to mesenchyme and less attention to epithelial effects on mesenchyme. In the present study, we used nascent organoids composed of human and mouse lung epithelial and mesenchymal cells to demonstrate that healthy lung epithelium dramatically represses transcriptional, contractile, and matrix synthetic functions of lung fibroblasts. Repression of fibroblast activation requires signaling via the bone morphogenetic protein (BMP) pathway. BMP signaling is diminished after epithelial injury
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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.