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Updated: Mar 16, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Platelets and coagulation in infection
Rachelle P Davis1, Sarah Miller-Dorey1, Craig N Jenne1
1Department of Microbiology, Immunology and Infectious Diseases, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, University of Calgary , Calgary, Alberta, Canada.
Insights
Disseminated intravascular coagulation (DIC) in sepsis worsens patient outcomes. New therapies targeting inflammation, platelets, and neutrophil extracellular traps (NETs) are needed to improve treatment for this complex condition.
Area of Science:
- Critical care medicine
- Hematology
- Immunology
Background:
- Disseminated intravascular coagulation (DIC) is a severe complication of sepsis, significantly increasing patient mortality and morbidity.
- DIC involves uncontrolled blood clot formation and consumption of clotting factors, leading to both thrombosis and hemorrhage.
- Current anticoagulant therapies for sepsis-associated DIC show limited efficacy, partly due to the immune system's role in initiating coagulation.
Purpose of the Study:
- To review current anticoagulant treatments for sepsis-associated DIC.
- To explore the role of inflammation, platelets, and neutrophil extracellular traps (NETs) in sepsis-induced coagulation.
- To discuss the development of future therapeutic strategies targeting these key mediators.
Main Methods:
- Literature review of current research on sepsis-associated DIC.
- Analysis of studies investigating the interplay between inflammation and coagulation.
- Examination of the role of platelets and NETs in infection-related coagulation.
Main Results:
- Sepsis-induced coagulation is complex, involving systemic inflammation.
- Platelets and NETs are identified as critical mediators in infection-driven coagulation processes.
- Existing anticoagulants have mixed outcomes, highlighting the need for novel approaches.
Conclusions:
- Effective treatment of sepsis-associated DIC requires addressing the interaction between inflammation and coagulation.
- Targeting platelet and NET-mediated coagulation pathways holds promise for future therapeutic development.
- Further research into novel anticoagulants that modulate immune responses is warranted.
Abstract:
Disseminated intravascular coagulation (DIC) is a frequent complication in sepsis that is associated with worse outcomes and higher mortality in patients. In addition to the uncontrolled generation of thrombi throughout the patient's vasculature, DIC often consumes large quantities of clotting factors leaving the patient susceptible to hemorrhaging. Owing to these complications, patients often receive anticoagulants to treat the uncontrolled clotting, often with mixed outcomes. This lack of success with the current array of anticoagulants can be partly explained by the fact that during sepsis clotting is often initiated by the immune system. Systemic inflammation has the capacity to activate and amplify coagulation and, as such, potential therapies for the treatment of sepsis-associated DIC need to address the interaction between inflammation and coagulation. Recent studies have suggested that platelets and neutrophil extracellular traps (NETs) are the key mediators of infection-induced coagulation. This review explores current anticoagulant therapies and discusses the development of future therapies to target platelet and NET-mediated coagulation.
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