ArticleJournal of inflammation (London, England)2025
Unfractionated heparin attenuated histone-induced pulmonary endothelial glycocalyx injury through Ang/Tie2 pathway.
Article in Journal of inflammation (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The trial behind it
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Who cites it
3 citing papers in PubMed.
- Unfractionated Heparin Attenuates Histone-Induced Pulmonary Endothelial Glycocalyx Injury: A Preliminary Study on the Roles of the ROCK Pathway and Heparanase‑1.Journal of inflammation research · 2026Article
- The Role of Histone Modifications in Acute Lung Injury: Molecular Mechanisms and Potential of Traditional Chinese Medicine Treatment.Journal of inflammation research · 2026Review
- Role of Tie-2 Axis in Sepsis: A Potential Therapeutic Target.Journal of cellular and molecular medicine · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
purposeThis study aimed to investigate the involvement of angiopoietin (Ang)/Tie2 pathway in mediating pulmonary endothelial glycocalyx injury in histone-induced acute lung injury in mice, and the protective mechanism of unfractionated heparin (UFH).
methodsTwenty-four male C57BL/6 mice (20-25 g), 8-12 weeks old, were randomly divided into control, histone, and histone + UFH groups. The histone (50 mg/kg) was administered via tail vein. UFH (400 U/kg) was administered 1 h after histone injection. The control group was administered by an equal amount of sterile saline solution. The lungs of all groups were harvested 4 h after the injection of histones or sterile saline.
resultsUFH attenuated histone-induced lung histopathological changes and edema. UFH alleviated pulmonary endothelial injury and glycocalyx shedding by reducing histone-induced low expression of thrombomodulin (TM) and decreased lung syndecan-1 levels. UFH improved histone-induced low mRNA expression of TM, syndecan-1, Ang-1, Tie2 and high expression of heparinase (HPA), Ang-2.
conclusionUFH may attenuate histone-induced lung injury and pulmonary endothelial glycocalyx degradation via the Ang/Tie2 pathway.
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