ReviewClinical science (London, England : 1979)2022
Dysregulated haemostasis in thrombo-inflammatory disease.
Review in Clinical science (London, England : 1979), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Biological clocks and blood clots in space: circadian disruption-induced modulation of thrombosis risk.Research and practice in thrombosis and haemostasis · 2026Pooled it
- Clinicopathological factors potentially relevant to pulmonary intravascular fibrin organisation in patients with COVID-19: an autopsy-based study.Virchows Archiv : an international journal of pathology · 2026Article
- Cardiovascular Complications of Anaplasmosis: A Case of Acute Pulmonary Embolism and Literature Review.Infectious disease reports · 2026Article
- Computational modeling of pro-inflammatory cytokine-enhanced blood coagulation.bioRxiv : the preprint server for biology · 2026Article
- Blood Coagulation in COVID-19: Systems-Biology Evidence, Clinical Implications, and Therapeutic Opportunities in an Evolving Pandemic.ACS omega · 2026Article
- Correlation analysis of the systemic immune-inflammation index with preoperative lower extremity deep venous thrombosis in patients with tibial fractures.Journal of orthopaedic surgery and research · 2026Article
- Computational Modeling of Pro-inflammatory Cytokine-Enhanced Blood Coagulation.Computational and structural biotechnology journal · 2026Article
- A Boolean Seven-Layer Platelet Decision Model Models Consistently the Logic and Semiquantitatively the Dynamics of Platelet Activation and Inhibition.Computational and structural biotechnology journal · 2026Article
- Network Controllability Reveals Key Mitigation Points for Tumor-Promoting Signaling in Tumor-Educated Platelets.International journal of molecular sciences · 2025Article
- Prolonged dysregulation of gene expression and biomarkers of coagulation, fibrinolysis, and endothelium in pediatric central nervous system malaria.BMC infectious diseases · 2025Article
- Molecular regulatory mechanisms of depression-related thrombosis risk.Journal of medical biochemistry · 2025Article
- Role of Clot Formation and Plasminogen Activation in Lower Urinary Tract Pathologies.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Tissue factor-dependent colitogenic CD4Nature communications · 2025Article
- Diabetic kidney disease: from pathogenesis to multimodal therapy-current evidence and future directions.Frontiers in medicine · 2025Review
- When viral myocarditis meets thrombosis tendency: deep analysis of a complex case report.Frontiers in cardiovascular medicine · 2025Article
- Apelin-13 as a novel diagnostic laboratory biomarker in thromboembolic disorders: a review of literature with prospective insights.International journal of emergency medicine · 2024Review
- The Influence of Circadian Rhythms on DNA Damage Repair in Skin Photoaging.International journal of molecular sciences · 2024Review
- Review
- Understanding the complex chromatin dynamics in primary human neutrophils during PMA-induced NET formation.Frontiers in immunology · 2024Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory disease is often associated with an increased incidence of venous thromboembolism in affected patients, although in most instances, the mechanistic basis for this increased thrombogenicity remains poorly understood. Acute infection, as exemplified by sepsis, malaria and most recently, COVID-19, drives 'immunothrombosis', where the immune defence response to capture and neutralise invading pathogens causes concurrent activation of deleterious prothrombotic cellular and biological responses. Moreover, dysregulated innate and adaptive immune responses in patients with chronic inflammatory conditions, such as inflammatory bowel disease, allergies, and neurodegenerative disorders, are now recognised to occur in parallel with activation of coagulation. In this review, we describe the detailed cellular and biochemical mechanisms that cause inflammation-driven haemostatic dysregulation, including aberrant contact pathway activation, increased tissue factor activity and release, innate immune cell activation and programmed cell death, and T cell-mediated changes in thrombus resolution. In addition, we consider how lifestyle changes increasingly associated with modern life, such as circadian rhythm disruption, chronic stress and old age, are increasingly implicated in unbalancing haemostasis. Finally, we describe the emergence of potential therapies with broad-ranging immunothrombotic functions, and how drug development in this area is challenged by our nascent understanding of the key molecular and cellular parameters that control the shared nodes of proinflammatory and procoagulant pathways. Despite the increasing recognition and understanding of the prothrombotic nature of inflammatory disease, significant challenges remain in effectively managing affected patients, and new therapeutic approaches to curtail the key pathogenic steps in immune response-driven thrombosis are urgently required.
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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.