ArticleJCI insight2022
Maladaptive functional changes in alveolar fibroblasts due to perinatal hyperoxia impair epithelial differentiation.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Apoptosis inhibition reprograms alveolar myofibroblasts toward ductal myofibroblasts.Cell reports · 2026Article
- Concerted action of gammaherpesvirus infection and moderate hyperoxia on lung structural development including effects on critical lung fibroblast functions in neonatal mice.Molecular and cellular pediatrics · 2026Article
- Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Rebalancing NTRK2 isoforms promotes vascular regeneration in bronchopulmonary dysplasia.Cell stem cell · 2026Article
- Temporal regulation of wnt signaling in alveolar development and regeneration: mechanistic insights and therapeutic advances in chronic lung diseases.Frontiers in cell and developmental biology · 2026Review
- Caffeine Protects Against Hyperoxia-Induced Structural Lung Injury and Restores Alveolar Development in Neonatal Rats.Antioxidants (Basel, Switzerland) · 2025Article
- Long-Term Maternal Exposure to Triclosan Provokes Pulmonary Fibrosis in Mouse Offspring.Environment & health (Washington, D.C.) · 2025Article
- Lung organoids: a new frontier in neonatology and paediatric respiratory medicine.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Isoform-Specific Roles of NTRK2 in Pulmonary Vascular Regeneration.bioRxiv : the preprint server for biology · 2025Article
- Impaired myofibroblast proliferation is a central feature of pathologic post-natal alveolar simplification.eLife · 2024Article
- Impaired Myofibroblast Proliferation is a Central Feature of Pathologic Post-Natal Alveolar Simplification.bioRxiv : the preprint server for biology · 2024Article
- Stem cells, cell therapies, and bioengineering in lung biology and diseases 2023.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- Bioinformatic analysis reveals the relationship between macrophage infiltration and Cybb downregulation in hyperoxia-induced bronchopulmonary dysplasia.Scientific reports · 2024Article
- Cell Cross-Talk in Alveolar Microenvironment: From Lung Injury to Fibrosis.American journal of respiratory cell and molecular biology · 2024Review
- Prenatal FGFR2 Signaling via PI3K/AKT Specifies the PDGFRAAmerican journal of respiratory cell and molecular biology · 2024Article
- Article
- CXCL10 deficiency limits macrophage infiltration, preserves lung matrix, and enables lung growth in bronchopulmonary dysplasia.Inflammation and regeneration · 2023Article
- Hedgehog and Platelet-derived Growth Factor Signaling Intersect during Postnatal Lung Development.American journal of respiratory cell and molecular biology · 2023Article
- Open questions in human lung organoid research.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Infants born prematurely worldwide have up to a 50% chance of developing bronchopulmonary dysplasia (BPD), a clinical morbidity characterized by dysregulated lung alveolarization and microvascular development. It is known that PDGFR alpha-positive (PDGFRA+) fibroblasts are critical for alveolarization and that PDGFRA+ fibroblasts are reduced in BPD. A better understanding of fibroblast heterogeneity and functional activation status during pathogenesis is required to develop mesenchymal population-targeted therapies for BPD. In this study, we utilized a neonatal hyperoxia mouse model (90% O2 postnatal days 0-7, PN0-PN7) and performed studies on sorted PDGFRA+ cells during injury and room air recovery. After hyperoxia injury, PDGFRA+ matrix and myofibroblasts decreased and PDGFRA+ lipofibroblasts increased by transcriptional signature and population size. PDGFRA+ matrix and myofibroblasts recovered during repair (PN10). After 7 days of in vivo hyperoxia, PDGFRA+ sorted fibroblasts had reduced contractility in vitro, reflecting loss of myofibroblast commitment. Organoids made with PN7 PDGFRA+ fibroblasts from hyperoxia in mice exhibited reduced alveolar type 1 cell differentiation, suggesting reduced alveolar niche-supporting PDGFRA+ matrix fibroblast function. Pathway analysis predicted reduced WNT signaling in hyperoxia fibroblasts. In alveolar organoids from hyperoxia-exposed fibroblasts, WNT activation by CHIR increased the size and number of alveolar organoids and enhanced alveolar type 2 cell differentiation.
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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.