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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

Insights

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.

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.

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