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Related Experiment Video

Updated: May 5, 2026

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
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Thrombin generation and atherosclerosis.

Jana Kalz1, Hugo ten Cate, Henri M H Spronk

  • 1Laboratory for Clinical Thrombosis and Haemostasis, Department of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University, P.O. Box 616, UNS50: Box8, 6200 MD, Maastricht, The Netherlands, jana.kalz@maastrichtuniversity.nl.

Journal of Thrombosis and Thrombolysis
|November 19, 2013
PubMed
Summary
This summary is machine-generated.

Thrombin, a key coagulation factor, promotes atherosclerosis by linking coagulation and inflammation. Anticoagulant therapies may offer protective effects against this cardiovascular disease.

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Area of Science:

  • Cardiovascular Research
  • Inflammation and Immunology
  • Hematology

Background:

  • Atherosclerosis is a leading global cause of mortality, significantly driven by inflammatory processes.
  • Thrombin, central to coagulation, also regulates inflammation via protease-activated receptors.
  • The interplay between coagulation and inflammation in atherosclerosis is increasingly recognized.

Purpose of the Study:

  • To explore the multifaceted roles of thrombin in the coagulation-inflammation axis of atherosclerosis.
  • To review mechanisms by which thrombin contributes to atherosclerotic plaque development and instability.
  • To discuss the potential of anticoagulant therapies in managing atherosclerosis.

Main Methods:

  • Analysis of human histological data from atherosclerotic lesions.
  • Review of animal studies investigating thrombin levels and atherosclerosis progression.
  • Examination of studies on direct oral anticoagulants (e.g., dabigatran, rivaroxaban) in atherosclerosis models.

Main Results:

  • Human data reveal significant coagulation activity in atherosclerotic lesions, correlating thrombin activity with plaque development and stability.
  • Animal studies demonstrate that elevated thrombin levels exacerbate atherosclerosis in Apolipoprotein E-deficient mice.
  • Administration of direct oral anticoagulants reduced atherosclerosis progression in experimental models.

Conclusions:

  • Thrombin shifts from a hemostasis regulator to an inflammation mediator in pathological conditions, disrupting protein C regulation.
  • Inflammatory activity, including cytokine and neutrophil extracellular trap activation, enhances thrombin generation while reducing anticoagulant protein C formation.
  • These pro-inflammatory and pro-thrombotic effects of thrombin are likely clinically relevant long-term, warranting further investigation into anticoagulant therapy's vascular side effects.