ArticleAmerican journal of physiology. Lung cellular and molecular physiology2023
Neonatal hyperoxia induces activated pulmonary cellular states and sex-dependent transcriptomic changes in a model of experimental bronchopulmonary dysplasia.
Article in American journal of physiology. Lung cellular and molecular physiology, 2023. 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, 23 citations in OpenAlex.
- Epigenetic programming in bronchopulmonary dysplasia: a framework linking early-life exposures to persistent lung disease-a narrative review.Pediatric research · 2026Review
- Mesenchyme-derived inflammation during the saccular stage recruits macrophages and alters lung development.JCI insight · 2026Article
- Sex-specific differences in lung mitochondrial function and injury in rats exposed to hyperoxia.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Article
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 2026Review
- Quantitative proteomics links mitochondrial dysfunction to metabolic changes and epithelial differentiation defects in hyperoxia-exposed neonatal airway cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- p53 maintains lineage fidelity during lung capillary injury-repair in neonatal hyperoxia.JCI insight · 2025Article
- Addressing Sex as a Biological Variable in Preclinical Models of Lung Disease: An Official American Thoracic Society Research Statement.American journal of respiratory and critical care medicine · 2025Article
- Specialized Pulmonary Vascular Cells in Development and Disease.Annual review of physiology · 2025Review
- The fungal microbiota modulate neonatal oxygen-induced lung injury.Microbiome · 2025Article
- Review
- 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
- Bioinformatic analysis reveals the relationship between macrophage infiltration and Cybb downregulation in hyperoxia-induced bronchopulmonary dysplasia.Scientific reports · 2024Article
- FAM134B deletion exacerbates apoptosis and epithelial-to-mesenchymal transition in rat lungs exposed to hyperoxia.iScience · 2024Article
- Endothelial deletion ofbioRxiv : the preprint server for biology · 2024Article
- Disrupted TGF-β signaling: a link between bronchopulmonary dysplasia and alveolar type 1 cells.The Journal of clinical investigation · 2024Article
- Modulation of recovery from neonatal hyperoxic lung injury by sex as a biological variable.Redox biology · 2023Article
- The Emerging Roles of Ferroptosis in Neonatal Diseases.Journal of inflammation research · 2023Review
- Remarkable sex-specific differences at single-cell resolution in neonatal hyperoxic lung injury.American journal of physiology. Lung cellular and molecular physiology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Hyperoxia disrupts lung development in mice and causes bronchopulmonary dysplasia (BPD) in neonates. To investigate sex-dependent molecular and cellular programming involved in hyperoxia, we surveyed the mouse lung using single cell RNA sequencing (scRNA-seq), and validated our findings in human neonatal lung cells in vitro. Hyperoxia-induced inflammation in alveolar type (AT) 2 cells gave rise to damage-associated transient progenitors (DATPs). It also induced a new subpopulation of AT1 cells with reduced expression of growth factors normally secreted by AT1 cells, but increased mitochondrial gene expression. Female alveolar epithelial cells had less EMT and pulmonary fibrosis signaling in hyperoxia. In the endothelium, expansion of Car4+ EC (Cap2) was seen in hyperoxia along with an emergent subpopulation of Cap2 with repressed VEGF signaling. This regenerative response was increased in females exposed to hyperoxia. Mesenchymal cells had inflammatory signatures in hyperoxia, with a new distal interstitial fibroblast subcluster characterized by repressed lipid biosynthesis and a transcriptomic signature resembling myofibroblasts. Hyperoxia-induced gene expression signatures in human neonatal fibroblasts and alveolar epithelial cells in vitro resembled mouse scRNA-seq data. These findings suggest that neonatal exposure to hyperoxia programs distinct sex-specific stem cell progenitor and cellular reparative responses that underpin lung remodeling in BPD.
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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.