ReviewFrontiers in immunology2026
Regulation of histones in thromboinflammation.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Epigenetic Regulation of the NET Formation-Blood-Brain Barrier Axis in Ischemic Stroke: Mechanisms, Therapeutic Targets and Translational Perspectives.Neurology international · 2026Review
- Multiple organ injury in septic rats under weightlessness.Frontiers in physiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular histones, once regarded solely as nuclear structural proteins, are now recognized as potent mediators of thrombo-inflammation which is the pathological interface of coagulation and immunity. Released during necrosis, apoptosis, and neutrophil extracellular trap (NET) formation, histones act as damage-associated molecular patterns (DAMPs), engaging receptors such as Toll-like receptors (TLR2, TLR4, TLR9) to trigger endothelial dysfunction, platelet activation, and cytokine release. Post-translational modifications (PTMs), including citrullination, acetylation, and methylation, further modulate histone immunogenicity, cytotoxicity, and procoagulant potential. These mechanisms amplify thrombin generation, impair anticoagulant pathways, and promote vascular permeability, positioning histones as central drivers of immunothrombosis in sepsis, stroke, ARDS, COVID-19, and autoimmune disorders. Circulating histones and nucleosomes are emerging as biomarkers for disease severity and prognosis. Therapeutic strategies targeting histones, such as neutralizing antibodies, heparin derivatives, PAD inhibitors, and activated protein C, show promise in mitigating histone-driven pathology. This review highlights mechanistic insights into histone biology and explores translational opportunities for targeted interventions at the intersection of inflammation and thrombosis.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.