ArticleAmerican journal of physiology. Lung cellular and molecular physiology2023
Remarkable sex-specific differences at single-cell resolution in neonatal hyperoxic lung injury.
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 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Incidence and risk factors of pulmonary hypertension in neonates with congenital diaphragmatic hernia: a systematic review and meta-analysis.Pediatric surgery international · 2025Pooled it
- Pilot study to validate endothelium collection from pulmonary artery balloon catheter in children.Pediatric research · 2026Article
- Mesenchyme-derived inflammation during the saccular stage recruits macrophages and alters lung development.JCI insight · 2026Article
- Attenuation of Experimental Bronchopulmonary Dysplasia by Dimethyl Fumarate.Pediatric research · 2026Article
- Sex-specific differences in lung mitochondrial function and injury in rats exposed to hyperoxia.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Article
- Neonatal Hyperoxia Induces Metabolic Reprogramming in Senescent Alveolar Macrophages, Leading to Persistent Lung Injury.Frontiers in bioscience (Landmark edition) · 2026Article
- The evolving pathophysiology of bronchopulmonary dysplasia.Physiological reviews · 2026Review
- Sex, hormones, and lung health.Physiological reviews · 2026Review
- Stage-specific neutrophil states in neonatal injury: from antimicrobial deficiency to pro-resolution repair.Frontiers in immunology · 2026Review
- Single-Cell Multiome Impact of Prenatal Heavy Metal Exposure on Early Airway Development.American journal of respiratory cell and molecular biology · 2026Article
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 2026Review
- Postnatal Abrogation of VEGFR2 Blocks Terminal Cap2 Differentiation by Preventing the Developmental Progression from a Capillary Intermediate Cell State.bioRxiv : the preprint server for biology · 2025Article
- 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
- Genetic variation in the activity of a TREM2-p53 signaling axis determines oxygen-induced lung injury.Nature immunology · 2025Article
- Docosahexaenoic Acid Supplementation in Postnatal Growth Restricted Rats Does Not Normalize Lung Function or PPARγ Activity.Biomolecules · 2025Article
- Endothelial Cpt1a Inhibits Neonatal Hyperoxia-Induced Pulmonary Vascular Remodeling by Repressing Endothelial-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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
- VEGF-A isoforms induce the expression of APLN in endothelial cells during human prenatal lung development.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Exposure to supraphysiological concentrations of oxygen (hyperoxia) predisposes to bronchopulmonary dysplasia (BPD), which is characterized by abnormal alveolarization and pulmonary vascular development, in preterm neonates. Neonatal hyperoxia exposure is used to recapitulate the phenotype of human BPD in murine models. Male sex is considered an independent predictor for the development of BPD, but the main mechanisms underlying sexually dimorphic outcomes are unknown. Our objective was to investigate sex-specific and cell-type specific transcriptional changes that drive injury in the neonatal lung exposed to hyperoxia at single-cell resolution and delineate the changes in cell-cell communication networks in the developing lung. We used single-cell RNA sequencing (scRNAseq) to generate transcriptional profiles of >35,000 cells isolated from the lungs of neonatal male and female C57BL/6 mice exposed to 95% [Formula: see text] between PND1-5 (saccular stage of lung development) or normoxia and euthanized at PND7 (alveolar stage of lung development). ScRNAseq identified 22 cell clusters with distinct populations of endothelial, epithelial, mesenchymal, and immune cells. Our data identified that the distal lung vascular endothelium (composed of aerocytes and general capillary endothelial cells) is exquisitely sensitive to hyperoxia exposure with the emergence of an intermediate capillary endothelial population with both general capillaries (gCap) and aerocytes or alveolar capillaries (aCap) markers. We also identified a myeloid-derived suppressor cell population from the lung neutrophils. Sex-specific differences were evident in all lung cell subpopulations but were striking among the lung immune cells. Finally, we identified that the specific intercellular communication networks and the ligand-receptor pairs that are impacted by neonatal hyperoxia exposure.
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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.