ReviewAntioxidants (Basel, Switzerland)2024
Role of Myeloperoxidase, Oxidative Stress, and Inflammation in Bronchopulmonary Dysplasia.
Review in Antioxidants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed.
- A Premature Rabbit Kitten Model for Evaluation of Bronchopulmonary Dysplasia Therapies Reproduces Myeloperoxidase-Associated Pathology and Therapeutic Responses.International journal of molecular sciences · 2026Article
- Early-life lung injury and the developing brain: a lung-brain axis perspective on neurodevelopmental disorders.Journal of neuroinflammation · 2026Review
- Expression and significance of miR-9-5p and GCH1 in neonates with bronchopulmonary dysplasia.Translational pediatrics · 2026Article
- Airway microbial dysbiosis and oxidative mitochondrial DNA damage in the development of bronchopulmonary dysplasia.ERJ open research · 2026Article
- Landscape of bronchopulmonary dysplasia: from mechanisms to management.Frontiers in pediatrics · 2026Article
- Stage-specific neutrophil states in neonatal injury: from antimicrobial deficiency to pro-resolution repair.Frontiers in immunology · 2026Review
- The Value of Cord Blood CXCL10 and MMP8 as Biomarkers in Predicting Bronchopulmonary Dysplasia- A Retrospective Cohort Study.International journal of general medicine · 2026Article
- Pharmacologic Inhibition of S-Nitrosoglutathione Reductase Prevents Hyperoxic Alveolar and Airway Disease in Newborn Mice.Biomedicines · 2025Article
- Inhibition of 5-hydroxyindoleacetic acid to reduce neutrophil extracellular trap production improves lung condition in chronic obstructive pulmonary disease mice.Annals of medicine · 2025Article
- Early predictive value of interleukin-6 and procalcitonin levels for bronchopulmonary dysplasia in preterm infants.Translational pediatrics · 2025Article
- Neutrophils in non-small cell lung cancer and immunotherapy with PD-1/PD-L1 inhibitors.Journal of translational medicine · 2025Review
- The Role of Mesenchymal Stromal Cells in the Treatment of Bronchopulmonary Dysplasia: A Multi-Prong Approach for a Heterogeneous Disease.Comprehensive physiology · 2025Review
- Predicting Future Respiratory Hospitalizations in Extremely Premature Neonates Using Transcriptomic Data and Machine Learning.Children (Basel, Switzerland) · 2025Article
- The Destructive Cycle in Bronchopulmonary Dysplasia: The Rationale for Systems Pharmacology Therapeutics.Antioxidants (Basel, Switzerland) · 2025Review
- Machine Learning Identification of Neutrophil Extracellular Trap-Related Genes as Potential Biomarkers and Therapeutic Targets for Bronchopulmonary Dysplasia.International journal of molecular sciences · 2025Article
- The role of potential oxidative biomarkers in the prognosis of intracerebral hemorrhage and the exploration antioxidants as possible preventive and treatment options.Frontiers in molecular biosciences · 2025Review
- Melatonin Activates KEAP1/NRF2/PTGS2 Pathway to Attenuate Hyperoxia-Driven Ferroptosis in Bronchopulmonary Dysplasia.Journal of inflammation research · 2025Article
- Effect Analysis of Extracellular Vesicles in the Treatment of Bronchopulmonary Dysplasia via Different Drug Delivery and Administration Routes.International journal of nanomedicine · 2025Review
- Molecular Approach of Oxidative Stress and Bronchopulmonary Dysplasia: Relationship of GSTM1 and GSTT1 Genes.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025Review
- Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Bronchopulmonary dysplasia (BPD) is a lung complication of premature births. The leading causes of BPD are oxidative stress (OS) from oxygen treatment, infection or inflammation, and mechanical ventilation. OS activates alveolar myeloid cells with subsequent myeloperoxidase (MPO)-mediated OS. Premature human neonates lack sufficient antioxidative capacity and are susceptible to OS. Unopposed OS elicits inflammation, endoplasmic reticulum (ER) stress, and cellular senescence, culminating in a BPD phenotype. Poor nutrition, patent ductus arteriosus, and infection further aggravate OS. BPD survivors frequently suffer from reactive airway disease, neurodevelopmental deficits, and inadequate exercise performance and are prone to developing early-onset chronic obstructive pulmonary disease. Rats and mice are commonly used to study BPD, as they are born at the saccular stage, comparable to human neonates at 22-36 weeks of gestation. The alveolar stage in rats and mice starts at the postnatal age of 5 days. Because of their well-established antioxidative capacities, a higher oxygen concentration (hyperoxia, HOX) is required to elicit OS lung damage in rats and mice. Neutrophil infiltration and ER stress occur shortly after HOX, while cellular senescence is seen later. Studies have shown that MPO plays a critical role in the process. A novel tripeptide, N-acetyl-lysyltyrosylcysteine amide (KYC), a reversible MPO inhibitor, attenuates BPD effectively. In contrast, the irreversible MPO inhibitor-AZD4831-failed to provide similar efficacy. Interestingly, KYC cannot offer its effectiveness without the existence of MPO. We review the mechanisms by which this anti-MPO agent attenuates BPD.
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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.