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Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
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Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Inflammation01:38

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Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...

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Related Experiment Video

Updated: May 24, 2026

Extracellular Vesicle Tissue Factor Activity Assay
03:53

Extracellular Vesicle Tissue Factor Activity Assay

Published on: December 29, 2023

Tissue factor-driven thrombin generation and inflammation in atherosclerosis.

Hugo ten Cate1

  • 1Laboratory for Clinical Thrombosis and Hemostasis, Department of Internal medicine and Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center, Maastricht, The Netherlands. h.tencate@maastrichtuniversity.nl

Thrombosis Research
|March 9, 2012
PubMed
Summary

Tissue factor and local thrombin generation play roles in atherosclerosis development. Anticoagulant interventions targeting these pathways show promise in reducing disease progression and inflammation in mouse models.

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Area of Science:

  • Cardiovascular Biology
  • Hematology
  • Pathophysiology

Background:

  • Tissue factor (TF) is a transmembrane receptor present in atherosclerotic lesions.
  • Local thrombin and fibrin generation may influence cellular functions in atherogenesis, including inflammation and cell proliferation.

Purpose of the Study:

  • To investigate the role of the coagulation system, particularly tissue factor and thrombin, in atherosclerosis.
  • To evaluate the impact of anticoagulant interventions on atherosclerosis progression and associated inflammation in experimental models.

Main Methods:

  • Studies in apoE(-/-) mice to assess atherosclerosis.
  • Evaluation of hypercoagulability and plaque phenotype.
  • Interventions included modulating tissue factor pathway inhibitor, and administration of selective factor Xa and thrombin inhibitors (rivaroxaban, dabigatran).

Main Results:

  • Hypercoagulability correlates with increased atherosclerosis in mice.
  • Overexpression of tissue factor pathway inhibitor reduced thrombogenicity and neo intima formation.
  • Selective inhibition of factor Xa and thrombin reduced inflammation in atherosclerotic mice.

Conclusions:

  • The local coagulation machinery, involving tissue factor and thrombin, is implicated in atherosclerosis.
  • Novel selective anticoagulants demonstrate potential in modifying atherosclerosis and associated inflammation.
  • Further clinical studies are warranted to explore the therapeutic potential of these agents in atherosclerosis.