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Dysregulated haemostasis in thrombo-inflammatory disease
Paula A Klavina1, Gemma Leon1,2, Annie M Curtis1
1Irish Centre of Vascular Biology, School of Pharmacy and Biomolecular Sciences, Royal College of Surgeons in Ireland, Dublin, Ireland.
Clinical Science (London, England : 1979)
|December 16, 2022
Summary
Inflammation triggers dangerous blood clots through immunothrombosis. Understanding these immune-driven clotting mechanisms is crucial for developing new therapies to manage inflammatory diseases and prevent thrombosis.
Area of Science:
- Immunology
- Hematology
- Pathophysiology
Background:
- Inflammatory diseases are linked to increased venous thromboembolism risk.
- The mechanisms behind inflammation-induced thrombogenicity are not fully understood.
- Acute infections (e.g., sepsis, COVID-19) and chronic conditions (e.g., IBD, allergies) involve 'immunothrombosis'.
Approach:
- This review details cellular and biochemical mechanisms of inflammation-driven hemostatic dysregulation.
- It examines aberrant contact pathway activation, increased tissue factor activity, and innate immune cell responses.
- The role of T cells in thrombus resolution and lifestyle factors (circadian disruption, stress, aging) are also considered.
Key Points:
- Inflammation activates coagulation through pathways like contact activation and tissue factor.
- Immune cell activation and programmed cell death contribute to prothrombotic states.
- T cells influence thrombus resolution, while lifestyle factors exacerbate hemostatic imbalance.
Conclusions:
- Developing therapies for immunothrombosis is challenging due to incomplete understanding of shared inflammatory and procoagulant pathways.
- New therapeutic strategies are urgently needed to target immune response-driven thrombosis in inflammatory diseases.
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