ArticlePediatric research2011
Hyperoxia impairs alveolar formation and induces senescence through decreased histone deacetylase activity and up-regulation of p21 in neonatal mouse lung.
Article in Pediatric research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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Who cites it
57 citing papers in PubMed, 87 citations in OpenAlex.
- Epigenetic programming in bronchopulmonary dysplasia: a framework linking early-life exposures to persistent lung disease-a narrative review.Pediatric research · 2026Review
- Unfolded protein response in bronchopulmonary dysplasia: mechanisms, pathways, and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Non-invasive respiratory support attenuates lung damage in a murine model of bronchopulmonary dysplasia.Frontiers in pediatrics · 2026Article
- Emerging roles of epigenetic regulators during lung development.Cell death & disease · 2025Review
- Cellular senescence in adult pulmonary hypertension: current state and future challenges.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- Decoding bronchopulmonary dysplasia in premature infants through an epigenetic lens.Frontiers in medicine · 2025Review
- Aging Lung: Molecular Drivers and Impact on Respiratory Diseases-A Narrative Clinical Review.Antioxidants (Basel, Switzerland) · 2024Review
- Senescence of lung mesenchymal stem cells of preterm infants by cyclic stretch and hyperoxia via p21.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Epigenetic modifications in the development of bronchopulmonary dysplasia: a review.Pediatric research · 2024Review
- GDF15 as a key disease target and biomarker: linking chronic lung diseases and ageing.Molecular and cellular biochemistry · 2024Review
- Activation of senescence in critically ill patients: mechanisms, consequences and therapeutic opportunities.Annals of intensive care · 2024Review
- Rad1 attenuates DNA double-strand breaks and cell cycle arrest in type II alveolar epithelial cells of rats with bronchopulmonary dysplasia.Molecular medicine (Cambridge, Mass.) · 2023Article
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- Timing and cell specificity of senescence drives postnatal lung development and injury.Nature communications · 2023Article
- Involvement of miRNA-34a regulated Krüppel-like factor 4 expression in hyperoxia-induced senescence in lung epithelial cells.Respiratory research · 2022Article
- Differential placental CpG methylation is associated with chronic lung disease of prematurity.Pediatric research · 2022Article
- The critical role of collagen VI in lung development and chronic lung disease.Matrix biology plus · 2021Review
- MicroRNA Signatures Associated with Bronchopulmonary Dysplasia Severity in Tracheal Aspirates of Preterm Infants.Biomedicines · 2021Article
- Senescence associated long non-coding RNA 1 regulates cigarette smoke-induced senescence of type II alveolar epithelial cells through sirtuin-1 signaling.The Journal of international medical research · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Alveolar development comprises the transition of lung architecture from saccules to gas-exchange units during late gestation and early postnatal development. Exposure to hyperoxia disrupts developmental signaling pathways and causes alveolar hypoplasia as seen in bronchopulmonary dysplasia affecting preterm human newborns. Expanding literature suggests that epigenetic changes caused by environmental triggers during development may lead to heritable changes in gene expression. Given recent data on altered histone deacetylase (HDAC) activity in lungs of humans and animal models with airspace enlargement/emphysema, we hypothesized that alveolar hypoplasia from hyperoxia exposure in neonatal mice is a consequence of cell cycle arrest and reduced HDAC activity and up-regulation of the cyclin-dependent kinase inhibitor, p21. We exposed newborn mice to hyperoxia and compared lung morphologic and epigenetic changes to room air controls. Furthermore, we pretreated a subgroup of animals with the macrolide antibiotic azithromycin (AZM), known to possess antiinflammatory properties. Our results showed that hyperoxia exposure resulted in alveolar hypoplasia and was associated with decreased HDAC1 and HDAC2 and increased p53 and p21 expression. Furthermore, AZM did not confer protection against hyperoxia-induced alveolar changes. These findings suggest that alveolar hypoplasia caused by hyperoxia is mediated by epigenetic changes affecting cell cycle regulation/senescence during lung development.
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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.