ReviewMolecular medicine reports2026
Research progress on neutrophil extracellular traps in sepsis‑induced coagulopathy (Review).
Review in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Targeting neutrophil extracellular traps in bacterial infections: mechanistic insights and translational perspectives.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis affects an estimated 166 million individuals globally with 21.4 million annual deaths and represents a notable public health challenge. Sepsis‑induced coagulopathy (SIC) is a marked complication of sepsis, characterized by dysregulated hemostasis and microvascular thrombosis. Neutrophil extracellular traps (NETs) are pivotal mediators linking innate immunity to thrombo‑inflammation in this process. The present review systematically examined the epidemiology and pathogenesis of SIC, the molecular mechanisms of NET release (suicidal, vital, mitochondrial and non‑canonical pathways) and the mechanistic pathways by which NETs regulate SIC. NETs disrupt endothelial integrity, amplify platelet activation, propagate coagulation cascades and suppress fibrinolysis, thereby establishing a self‑amplifying cycle that accelerates progression to disseminated intravascular coagulation and multiple organ failure. Furthermore, the present review highlighted current therapeutic strategies targeting NETs, including inhibition of NET synthesis, acceleration of NET clearance and disruption of platelet‑neutrophil interactions. Elucidating the central role of NETs in SIC pathophysiology may facilitate the development of novel biomarkers and precision therapeutic interventions for this life‑threatening condition.
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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.