ArticleNature communications2017
Hyperoxia causes miR-34a-mediated injury via angiopoietin-1 in neonatal lungs.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 127 citations in OpenAlex.
- Attenuation of Experimental Bronchopulmonary Dysplasia by Dimethyl Fumarate.Pediatric research · 2026Article
- Neonatal kidney injury in the hyperoxia-induced bronchopulmonary dysplasia mouse models: effect on morphology and biomarkers.Pediatric research · 2026Article
- GINS4 Promotes Neonatal Bronchopulmonary Dysplasia via Driving Phosphorylation and Acetylation of p65 NF-κB.Molecular biotechnology · 2026Article
- miR-21-5p attenuates hyperoxia-induced lung injury by modulating YAP1-dependent ferroptosis.Frontiers in pharmacology · 2026Article
- The evolving pathophysiology of bronchopulmonary dysplasia.Physiological reviews · 2026Review
- Unraveling Optimal Dose and Responsive Markers for Human Cord Blood Derived Mononuclear Cells in Alleviating Bronchopulmonary Dysplasia in Neonatal Mice.International journal of stem cells · 2025Article
- Establishment of a neonatal rat model of sequential hyperoxic hypoxia to recapitulate clinical progression of bronchopulmonary dysplasia-associated pulmonary hypertension.Intensive care medicine experimental · 2025Article
- Current and Emerging Therapies for Prevention and Treatment of Bronchopulmonary Dysplasia in Preterm Infants.Paediatric drugs · 2025Review
- [Expression and regulatory mechanism of miR-34a in neonatal rat model of bron-chopulmonary dysplasia induced by hyperoxia].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025Article
- Decoding STAT3: a new frontier in understanding and treating hyperoxic lung injury.Frontiers in immunology · 2025Review
- Roles of microRNAs in acute lung injury and acute respiratory distress syndrome: mechanisms and clinical potential.Frontiers in immunology · 2025Review
- Implication of m6A Methylation Regulators in the Immune Microenvironment of Bronchopulmonary Dysplasia.Biochemical genetics · 2024Article
- A novel circRNA-miRNA-mRNA regulatory axis as a sex-specific biological variable in bronchopulmonary dysplasia.NAR molecular medicine · 2024Article
- Epigenetics and bronchopulmonary dysplasia: unraveling the complex interplay and potential therapeutic implications.Pediatric research · 2024Article
- miRNA Signatures in Bronchopulmonary Dysplasia: Implications for Biomarkers, Pathogenesis, and Therapeutic Options.Frontiers in bioscience (Landmark edition) · 2024Review
- Article
- Recruitment of PVT1 Enhances YTHDC1-Mediated m6A Modification of IL-33 in Hyperoxia-Induced Lung Injury During Bronchopulmonary Dysplasia.Inflammation · 2024Article
- Emerging role of cellular senescence in normal lung development and perinatal lung injury.Chinese medical journal pulmonary and critical care medicine · 2024Article
- Amphiregulin Exerts Proangiogenic Effects in Developing Murine Lungs.Antioxidants (Basel, Switzerland) · 2024Article
- Investigation of the miRNA-mRNA Regulatory Circuits and Immune Signatures Associated with Bronchopulmonary Dysplasia.Journal of inflammation research · 2024Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
Abstract
Hyperoxia-induced acute lung injury (HALI) is a key contributor to the pathogenesis of bronchopulmonary dysplasia (BPD) in neonates, for which no specific preventive or therapeutic agent is available. Here we show that lung micro-RNA (miR)-34a levels are significantly increased in lungs of neonatal mice exposed to hyperoxia. Deletion or inhibition of miR-34a improves the pulmonary phenotype and BPD-associated pulmonary arterial hypertension (PAH) in BPD mouse models, which, conversely, is worsened by miR-34a overexpression. Administration of angiopoietin-1, which is one of the downstream targets of miR34a, is able to ameliorate the BPD pulmonary and PAH phenotypes. Using three independent cohorts of human samples, we show that miR-34a expression is increased in type 2 alveolar epithelial cells in neonates with respiratory distress syndrome and BPD. Our data suggest that pharmacologic miR-34a inhibition may be a therapeutic option to prevent or ameliorate HALI/BPD in neonates.
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