ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018
Lung omics signatures in a bronchopulmonary dysplasia and pulmonary hypertension-like murine model.
Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Investigating mitophagy mechanisms in bronchopulmonary dysplasia through bioinformatics.Pediatric research · 2026Article
- Mitochondrial quality control mechanisms as molecular targets for impaired lung development: from fetuses to neonates.Respiratory research · 2025Review
- Predicting Future Respiratory Hospitalizations in Extremely Premature Neonates Using Transcriptomic Data and Machine Learning.Children (Basel, Switzerland) · 2025Article
- Research progress of microvascular development in bronchopulmonary dysplasia.Pediatric investigation · 2024Review
- A novel circRNA-miRNA-mRNA regulatory axis as a sex-specific biological variable in bronchopulmonary dysplasia.NAR molecular medicine · 2024Article
- New insights into the natural history of bronchopulmonary dysplasia from proteomics and multiplexed immunohistochemistry.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Pathogenesis of Bronchopulmonary Dysplasia: Role of Oxidative Stress from 'Omics' Studies.Antioxidants (Basel, Switzerland) · 2022Review
- Effects of Hyperoxia and Hyperoxic Oscillations on the Proteome of Murine Lung Microvascular Endothelium.Antioxidants (Basel, Switzerland) · 2022Article
- Intratracheal administration of umbilical cord-derived mesenchymal stem cells attenuates hyperoxia-induced multi-organ injuryWorld journal of stem cells · 2022Article
- Daily Intraperitoneal Administration of Rosiglitazone Does Not Improve Lung Function or Alveolarization in Preterm Rabbits Exposed to Hyperoxia.Pharmaceutics · 2022Article
- Vitamin D Ameliorates Apoptosis and Inflammation by Targeting the Mitochondrial and MEK1/2-ERK1/2 Pathways in Hyperoxia-Induced Bronchopulmonary Dysplasia.Journal of inflammation research · 2022Article
- Patho-mechanisms of the origins of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2021Review
- EndothelialAntioxidants (Basel, Switzerland) · 2021Article
- A clinical study on plasma biomarkers for deciding the use of adjuvant corticosteroid therapy in bronchopulmonary dysplasia of premature infants.International journal of medical sciences · 2021Observational
- Biomarkers of Oxidative Stress for Neonatal Lung Disease.Frontiers in pediatrics · 2021Review
- An Innovative Model of Bronchopulmonary Dysplasia in Premature Infants.Frontiers in pediatrics · 2020Article
- Human induced pluripotent stem cells ameliorate hyperoxia-induced lung injury in a mouse model.American journal of translational research · 2020Article
- Endothelial-to-mesenchymal transition: Pathogenesis and therapeutic targets for chronic pulmonary and vascular diseases.Biochemical pharmacology · 2019Review
- Oxidative Stress and Bronchopulmonary Dysplasia: Evidences From Microbiomics, Metabolomics, and Proteomics.Frontiers in pediatrics · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Bronchopulmonary dysplasia (BPD), the most common chronic lung disease in infants, is associated with long-term morbidities, including pulmonary hypertension (PH). Importantly, hyperoxia causes BPD and PH; however, the underlying mechanisms remain unclear. Herein, we performed high-throughput transcriptomic and proteomic studies using a clinically relevant murine model of BPD with PH. Neonatal wild-type C57BL6J mice were exposed to 21% oxygen (normoxia) or 70% oxygen (hyperoxia) during postnatal days (PNDs) 1-7. Lung tissues were collected for proteomic and genomic analyses on PND 7, and selected genes and proteins were validated by real-time quantitative PCR and immunoblotting analysis, respectively. Hyperoxia exposure dysregulated the expression of 344 genes and 21 proteins. Interestingly, hyperoxia downregulated genes involved in neuronal development and maturation in lung tissues. Gene set enrichment and gene ontology analyses identified apoptosis, oxidoreductase activity, plasma membrane integrity, organ development, angiogenesis, cell proliferation, and mitophagy as the predominant processes affected by hyperoxia. Furthermore, selected deregulated proteins strongly correlated with the expression of specific genes. Collectively, our results identified several potential therapeutic targets for hyperoxia-mediated BPD and PH in infants.
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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.