ArticleRedox biology2023
Modulation of recovery from neonatal hyperoxic lung injury by sex as a biological variable.
Article in Redox biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 3 citations in OpenAlex.
- Smaller coronary artery size in adults born preterm.Pediatric research · 2026Article
- Multiscale computational modeling of the cardiopulmonary consequences of postnatal hyperoxia with implications for preterm-born children.Biomechanics and modeling in mechanobiology · 2026Article
- Unfolded protein response in bronchopulmonary dysplasia: mechanisms, pathways, and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Multiscale Computational Modeling of the Cardiopulmonary Consequences of Postnatal Hyperoxia with Implications for Preterm Born Children.bioRxiv : the preprint server for biology · 2025Article
- Modeling Dysplastic and Functional Lung Alveolar Repair after Influenza Infection.Journal of visualized experiments : JoVE · 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
- Role of sex as a biological variable in neonatal alveolar macrophages.Redox biology · 2024Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Recovery from lung injury during the neonatal period requires the orchestration of many biological pathways. The modulation of such pathways can drive the developing lung towards proper repair or persistent maldevelopment that can lead to a disease phenotype. Sex as a biological variable can regulate these pathways differently in the male and female lung exposed to neonatal hyperoxia. In this study, we assessed the contribution of cellular diversity in the male and female neonatal lung following injury. Our objective was to investigate sex and cell-type specific transcriptional changes that drive repair or persistent injury in the neonatal lung and delineate the alterations in the immune-endothelial cell communication networks using single cell RNA sequencing (sc-RNAseq) in a murine model of hyperoxic injury. We generated transcriptional profiles of >55,000 cells isolated from the lungs of postnatal day 1 (PND 1; pre-exposure), PND 7, and PND 21neonatal male and female C57BL/6 mice exposed to 95 % FiO
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Registered trials
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