ArticleCell death discovery2023
Neutrophil extracellular traps contribute to immunothrombosis formation via the STING pathway in sepsis-associated lung injury.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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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.
The trial behind it
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Who cites it
59 citing papers in PubMed, 73 citations in OpenAlex.
- Neutrophil extracellular traps in cardiovascular disease: Mechanisms and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Neutrophils promote endothelial cell activation in pediatric Mycoplasma pneumoniae pneumonia.JCI insight · 2026Article
- A Sulfonamide Intermediate Elicits Therapeutic Effect Against Sepsis by Enhancing Neutrophil Maturation.Journal of cellular and molecular medicine · 2026Article
- The NETs-cGAS-STING Axis in Ischemic Stroke: Linking Neutrophil-Microglia Crosstalk, Immunothrombosis, and Neuroinflammation.Molecular neurobiology · 2026Review
- Pleural fluid neutrophil extracellular traps are associated with disease severity and risk of 1-year mortality in pleural infection: an observational, international, multicohort study (TORPIDS-3).The European respiratory journal · 2026Observational
- Expansion of CD101⁻ neutrophils drives susceptibility to hyperyersiniabactin-producingInfection and immunity · 2026Article
- Research progress on neutrophil extracellular traps in sepsis‑induced coagulopathy (Review).Molecular medicine reports · 2026Review
- Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.Biomarker research · 2026Review
- Abdominal Symptoms During the Febrile Phase Indicate Profound Innate Immune Responses in Dengue.Biology · 2026Article
- Alveolar macrophage-neutrophil crosstalk in acute lung injury: mechanisms, feedback loops, and therapeutic opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Ferroptosis, orchestrated by GPX4 downregulation, serves as a critical mediator of neutrophil extracellular trap-driven pathology in hypoxic pulmonary edema.Apoptosis : an international journal on programmed cell death · 2026Article
- A multi-biomarker nomogram based on miR-155-5p and NETs predicting deep vein thrombosis risk stratification.Thrombosis journal · 2026Article
- Type 2 immune history imprints local training in nerve and airway associated interstitial macrophages (NAMs) for disease tolerance during lethal respiratory viral infection.Research square · 2026Article
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Mitochondria as Inducers of Neutrophil Extracellular Traps.Inflammation · 2026Review
- Circadian Control of Neutrophils Drives Collateral Perfusion and Stroke Outcome.Circulation research · 2026Article
- Machine learning integration of bulk and single-cell RNA-Seq data reveals COPS2 as a central immune regulator in deep vein thrombosis.American journal of translational research · 2026Article
- Extracellular vesicles as emerging platforms for modulating innate immune responses in sepsis-associated acute lung injury.Frontiers in immunology · 2026Review
- Neutrophils and neutrophil extracellular traps in ischaemia-reperfusion injury: pathophysiological roles and therapeutic potential.Burns & trauma · 2026Review
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Neutrophil extracellular traps (NETs) are involved in the activation and dysfunction of multiple overlapping and interacting pathways, including the immune response to injury, inflammation, and coagulation, which contribute to the pathogenesis of sepsis-induced acute lung injury (SI-ALI). However, how NETs mediate the relationship between inflammation and coagulation has not been fully clarified. Here, we found that NETs, through stimulator of interferon genes (STING) activation, induced endothelial cell damage with abundant production of tissue factor (TF), which magnified the dysregulation between inflammatory and coagulant responses and resulted in poor prognosis of SI-ALI model mice. Disruption of NETs and inhibition of STING improved the outcomes of septic mice and reduced the inflammatory response and coagulation. Furthermore, Toll-like receptor 2 (TLR2) on the surface of endothelial cells was involved in the interaction between NETs and the STING pathway. Collectively, these findings demonstrate that NETs activate the coagulant cascade in endothelial cells in a STING-dependent manner in the development of SI-ALI.
Identifiers
What OpenQuestion 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 OpenQuestion graph.