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Related Experiment Video

Updated: Apr 11, 2026

Author Spotlight: High-Sensitivity Tissue Factor Activity Assay for Plasma Diagnosis
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Tissue Factor and Atherothrombosis.

Kohei Tatsumi1, Nigel Mackman

  • 1Department of Medicine, Division of Hematology and Oncology, McAllister Heart Institute, Thrombosis and Hemostasis Group,University of North Carolina at Chapel Hill.

Journal of Atherosclerosis and Thrombosis
|May 29, 2015
PubMed
Summary
This summary is machine-generated.

Atherosclerosis involves lipid buildup in arteries, leading to atherothrombosis and events like heart attack. Targeting pathological tissue factor (TF) expression, not all TF, may prevent thrombosis without harming hemostasis.

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Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Pathology

Background:

  • Atherosclerosis is characterized by arterial lipid accumulation, potentially leading to atherothrombosis, myocardial infarction, and stroke.
  • Key risk factors like hyperlipidemia, diabetes, smoking, and hypertension elevate tissue factor (TF) expression.
  • TF is abundant in atherosclerotic plaques and on microvesicles (MVs), with oxidized LDL exacerbating TF induction in monocytes.

Purpose of the Study:

  • To investigate the role of tissue factor (TF) in atherothrombosis.
  • To explore therapeutic strategies targeting TF for reducing atherothrombotic events.

Main Methods:

  • Review of literature on atherosclerosis, atherothrombosis, and tissue factor (TF) expression.
  • Analysis of TF sources in atherosclerotic plaques and circulation (monocytes, MVs).
  • Evaluation of potential therapeutic interventions, including TF inhibition and statin effects.

Main Results:

  • TF within atherosclerotic plaques is a major driver of thrombosis post-rupture.
  • TF on circulating monocytes and MVs may also contribute to thrombosis.
  • Statins demonstrate potential by reducing TF expression in plaques and monocytes.

Conclusions:

  • Direct inhibition of the TF/factor VIIa complex is unlikely to be effective due to its role in hemostasis.
  • Selective blockade of pathological TF, sparing protective TF, offers a promising strategy for atherothrombosis treatment.
  • Further research is required to develop safe and effective methods for reducing pathological TF expression and preventing atherothrombosis.