ArticleJournal of inflammation research2023
Protectin DX Relieve Hyperoxia-induced Lung Injury by Protecting Pulmonary Endothelial Glycocalyx.
Article in Journal of inflammation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Tocotrienol metabolites redirect lipid mediator production in innate immune cells towards inflammation resolution.Acta pharmaceutica Sinica. B · 2026Article
- Protectin DX reduces inflammatory pain initiated by superoxide anion in mice: targeting leukocyte recruitment, oxidative stress, cytokine production and TRPV1Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Heart-Lung Interactions in Gas Exchange: From Physiology to Pathophysiology.Comprehensive Physiology · 2026Review
- Resolvin D1 improves bleomycin-induced alveolar maturation arrest in newborn rats.Scientific reports · 2025Article
- Establishment and Evaluation of Cell Models for Bronchopulmonary Dysplasia: Challenges and Prospects.The clinical respiratory journal · 2025Review
- Multienzyme active melanin nanodots for antioxidant-immunomodulatory therapy of hyperoxia lung injury.Materials today. Bio · 2025Article
- [Role of reactive oxygen species/silent information regulator 1 in hyperoxia-induced bronchial epithelial cell injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- IRF4-mediated Treg phenotype switching can aggravate hyperoxia-induced alveolar epithelial cell injury.BMC pulmonary medicine · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Bronchopulmonary dysplasia (BPD) is a common chronic lung disease in premature infants with limited treatments and poor prognosis. Damaged endothelial glycocalyx leads to vascular permeability, lung edema and inflammation. However, whether hyperoxia increases neonatal pulmonary microvascular permeability by degrading the endothelial glycocalyx remains unknown. Methods: Newborn mice were maintained in 60-70% O Results: Hyperoxia exposure for 7 days led to neonatal mice alveolar simplification with less radial alveolar count (RAC), mean linear intercept (MLI) and mean alveolar diameter (MAD) compared to the control group. Hyperoxia exposure increased lung vascular permeability with more fluid and proteins and inflammatory factors, including TNF-α and IL-1β, in bronchoalveolar lavage fluid while reducing the heparan sulfate (HS), the most abundant component of the endothelial glycocalyx, in the pulmonary endothelial cells. PDX relieve these changes. PDX attenuated hyperoxia-induced high expression of heparanase (HPA), the endoglycosidase that shed endothelial glycocalyx, p-P65, P65, and low expression of SIRT1. BOC-2 and EX527 abolished the affection of PDX both in vivo and intro. Conclusion: In summary, our findings indicate that PDX treatment relieves hyperoxia-induced alveolar simplification, vascular leakage and lung inflammation by attenuating pulmonary endothelial glycocalyx injury via the SIRT1/NF-κB/ HPA pathway.
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