ArticleBMC pulmonary medicine2025
By activating endothelium histone H4 mediates oleic acid-induced acute respiratory distress syndrome.
Article in BMC pulmonary medicine, 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 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
3 citing papers in PubMed.
- Role of post-translational modifications in modulating histone reactivity in the extracellular environment.Biochemical Society transactions · 2026Review
- Source-renewing ectopic ApoB-TRL lipolysis in non-resolving ARDS: a testable spatial hypothesis.Frontiers in immunology · 2026Article
- The Role of Histone Modifications in Acute Lung Injury: Molecular Mechanisms and Potential of Traditional Chinese Medicine Treatment.Journal of inflammation research · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
objectiveThis study investigated pathogenic role and mechanism of extracellular histone H4 during oleic acid (OA)-induced acute respiratory distress syndrome (ARDS).
methodsARDS was induced by intravenous injection of OA in mice, and evaluated by blood gas, pathological analysis, lung edema, and survival rate. Heparan sulfate (HS) degradation was evaluated using immunofluorescence and flow cytometry. The released von Willebrand factor (vWF) was measured using ELISA. P-selectin translocation and neutrophil infiltration were measured via immunohistochemical analysis. Changes in VE-cadherin were measured by western blot. Blocking antibodies against TLRs were used to investigate the signaling pathway.
resultsHistone H4 in plasma and BALF increased significantly after OA injection. Histone H4 was closely correlated with the OA dose, which determined the ARDS severity. Pretreatment with histone H4 further aggravated pulmonary edema and death rate, while anti-H4 antibody exerted obvious protective effects. Histone H4 directly activated the endothelia. Endothelial activation was evidently manifested as HS degradation, release of vWF, P-selectin translocation, and VE-Cadherin reduction. The synergistic stimulus of activated endothelia was required for effective neutrophil activation by histone H4. Both TLRs and calcium mediated histone H4-induced endothelial activation.
conclusionsHistone H4 is a pro-inflammatory and pro-thrombotic molecule in OA-induced ARDS in mice.
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