ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Mouse lung development and NOX1 induction during hyperoxia are developmentally regulated and mitochondrial ROS dependent.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 74 citations in OpenAlex.
- Role of ROS, soluble guanylate cyclase and cGMP in mouse lung development during hyperoxia.American journal of physiology. Heart and circulatory physiology · 2026Article
- Effects of Di(2-ethylhexyl) phthalate (DEHP) and hyperoxia on cardiovascular development in newborn rats.Pediatric research · 2026Article
- Mitochondrial quality control mechanisms as molecular targets for impaired lung development: from fetuses to neonates.Respiratory research · 2025Review
- Caffeine Protects Against Hyperoxia-Induced Structural Lung Injury and Restores Alveolar Development in Neonatal Rats.Antioxidants (Basel, Switzerland) · 2025Article
- Effect of NADPH oxidase inhibitor apocynin on human lung cancer A549 cells via Bcl-2, Bax, caspase-3, and NF-κB signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Whole genome transcriptomics reveal distinct atrial versus ventricular responses to neonatal hyperoxia.American journal of physiology. Heart and circulatory physiology · 2025Article
- Oxidative stress in pediatric diseases associated with the origin of life and growth and development.Frontiers in cell and developmental biology · 2025Review
- Molecular mechanisms underlying methotrexate-induced intestinal injury and protective strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Decreased Liver Kinase B1 Expression and Impaired Angiogenesis in a Murine Model of Bronchopulmonary Dysplasia.American journal of respiratory cell and molecular biology · 2024Article
- Beyond Bronchopulmonary Dysplasia: A Comprehensive Review of Chronic Lung Diseases in Neonates.Cureus · 2024Review
- Bronchopulmonary Dysplasia and Cell Senescence: A Case of Old Lungs in Young Infants?American journal of respiratory cell and molecular biology · 2024Article
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- O-linked N-acetylglucosamine affects mitochondrial homeostasis by regulating Parkin-dependent mitophagy in hyperoxia-injured alveolar type II cells injury.Respiratory research · 2023Article
- Oxygen and mechanical stretch in the developing lung: risk factors for neonatal and pediatric lung disease.Frontiers in medicine · 2023Review
- Neonatal Hyperoxia Activates Activating Transcription Factor 4 to Stimulate Folate Metabolism and Alveolar Epithelial Type 2 Cell Proliferation.American journal of respiratory cell and molecular biology · 2022Article
- Preventable ATII Proliferation after Hyperoxia: The "Tempo" of Folate Metabolism in the Neonatal Lung.American journal of respiratory cell and molecular biology · 2022Article
- The Role of Sphingolipid Signaling in Oxidative Lung Injury and Pathogenesis of Bronchopulmonary Dysplasia.International journal of molecular sciences · 2022Review
- Sphingosine kinase 1 regulates lysyl oxidase through STAT3 in hyperoxia-mediated neonatal lung injury.Thorax · 2022Article
- PGC-1α activity and mitochondrial dysfunction in preterm infants.Frontiers in physiology · 2022Review
- Molecular Mechanism of Caffeine in Preventing Bronchopulmonary Dysplasia in Premature Infants.Frontiers in pediatrics · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Animal models demonstrate that exposure to supraphysiological oxygen during the neonatal period compromises both lung and pulmonary vascular development, resulting in a phenotype comparable to bronchopulmonary dysplasia (BPD). Our prior work in murine models identified postnatal maturation of antioxidant enzyme capacities as well as developmental regulation of mitochondrial oxidative stress in hyperoxia. We hypothesize that consequences of hyperoxia may also be developmentally regulated and mitochondrial reactive oxygen species (ROS) dependent. To determine whether age of exposure impacts the effect of hyperoxia, neonatal mice were placed in 75% oxygen for 72 h at either postnatal day 0 (early postnatal) or day 4 (late postnatal). Mice exposed to early, but not late, postnatal hyperoxia demonstrated decreased alveolarization and septation, increased muscularization of resistance pulmonary arteries, and right ventricular hypertrophy (RVH) compared with normoxic controls. Treatment with a mitochondria-specific antioxidant, (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl)triphenylphosphonium chloride (mitoTEMPO), during early postnatal hyperoxia protected against compromised alveolarization and RVH. In addition, early, but not late, postnatal hyperoxia resulted in induction of NOX1 expression that was mitochondrial ROS dependent. Because early, but not late, exposure resulted in compromised lung and cardiovascular development, we conclude that the consequences of hyperoxia are developmentally regulated and decrease with age. Attenuated disease in mitoTEMPO-treated mice implicates mitochondrial ROS in the pathophysiology of neonatal hyperoxic lung injury, with potential for amplification of ROS signaling through NOX1 induction. Furthermore, it suggests a potential role for targeted antioxidant therapy in the prevention or treatment of BPD.
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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.