ReviewThrombosis research2014
Crosstalk between the coagulation and complement systems in sepsis.
Review in Thrombosis research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 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
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
91 citing papers in PubMed, 148 citations in OpenAlex.
- Complement system component dysregulation is a distinctive feature of COVID-19 disease: a prospective and comparative analysis of patients admitted to the emergency department for suspected COVID-19 disease.Journal of thrombosis and thrombolysis · 2022Trial
- Plasma proteomic profiling of septic shock and acute pancreatitis identifies shared signatures and disease-specific pathways.Scientific reports · 2026Article
- Time-Series modeling for predicting mortality risk in intensive care unit patients with pulmonary inflammation.Frontiers in medicine · 2026Article
- Machine learning identifies clinical sepsis phenotypes that translate to the plasma proteome.Infection · 2025Article
- A novel long-acting C5a-blocking cyclic peptide prevents sepsis-induced organ dysfunction via effective blockade of the inflammatory cascade.Signal transduction and targeted therapy · 2025Article
- Deficiencies of carboxypeptidase N and carboxypeptidase B2 have opposite effects in a virulent mouse E. coli sepsis model.Journal of thrombosis and haemostasis : JTH · 2025Article
- Disseminated intravascular coagulation.Journal of intensive care · 2025Review
- Article
- Recent Advances in Pathogenesis and Anticoagulation Treatment of Sepsis-Induced Coagulopathy.Journal of inflammation research · 2025Review
- Transcriptomics changes of calcitonin gene-related peptide in mitigating lipopolysaccharide-induced septic cardiomyopathy.Scientific reports · 2024Article
- The dysfunction of complement and coagulation in diseases: the implications for the therapeutic interventions.MedComm · 2024Review
- Pathophysiological dynamics in the contact, coagulation, and complement systems during sepsis: Potential targets for nafamostat mesilate.Journal of intensive medicine · 2024Review
- The Interaction of Complement and Intrinsic Coagulation System: A Comparative Study between COVID-19 and Bacterial Sepsis Patients.Journal of clinical medicine · 2024Article
- Organ crosstalk and dysfunction in sepsis.Annals of intensive care · 2024Review
- The association of platelet count, high-density lipoprotein cholesterol, and platelet/high-density lipoprotein cholesterol ratio with serum soluble Klotho.Lipids in health and disease · 2024Article
- Applications of peptides in nanosystems for diagnosing and managing bacterial sepsis.Journal of biomedical science · 2024Review
- Low-frequency inherited complement receptor variants are associated with purpura fulminans.Blood · 2024Article
- The value of the platelet/high-density lipoprotein cholesterol ratio in predicting depression and its cardiovascular disease mortality: a population-based observational study.Frontiers in endocrinology · 2024Observational
- Article
- Unraveling the Intricate Web: Complement Activation Shapes the Pathogenesis of Sepsis-Induced Coagulopathy.Journal of innate immunity · 2024Review
31 more citing papers are in PubMed but not listed here.
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
Abstract
Sepsis is a potent activator of the hemostatic and complement systems. While local activation of these proteolytic cascades contributes to the host defense, their uncontrolled systemic activation has major tissue damaging effects that lead to multiple organ failure and death. We have extensively studied the activation of complement and coagulation cascades in experimental sepsis using baboons challenged with live bacteria, such as Gram-negative Escherichia coli or Gram-positive Staphylococcus aureus and Bacillus anthracis, or with the bacterial product peptidoglycan. We observed that these challenges rapidly induce disseminated intravascular coagulation and robust complement activation. We applied a potent C3 convertase inhibitor, compstatin, which prevented sepsis-induced complement activation, reduced thrombocytopenia, decreased the coagulopathic responses, and preserving the endothelial anticoagulant properties. Overall, our work demonstrates that live bacteria and bacterial products activate the complement and coagulation cascades, and that blocking formation of complement activation products, especially during the organ failure stage of severe sepsis could be a potentially important therapeutic strategy.
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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.