Sources of tissue factor that contribute to thrombosis after rupture of an atherosclerotic plaque

Thromb Res. 2012 May;129 Suppl 2(Suppl 2):S30-3. doi: 10.1016/j.thromres.2012.02.026. Epub 2012 Mar 22.

Abstract

Hyperlipidemia leads to the formation of oxidized LDL (oxLDL), vessel dysfunction, atherosclerotic disease, and ultimately to plaque rupture and thrombosis. OxLDL induces tissue factor (TF) expression in various cell types, including monocytes and macrophages. High levels of TF are present in atherosclerotic plaques and this represents that major source of TF that triggers thrombosis after plaque rupture. In addition, increased levels of "circulating TF" are observed in hyperlipidemic animals and patients. This is due to induced TF expression in monocytes and release of monocyte-derived, TF(+) microparticles, which represents a minor source of TF that likely contributes to thrombosis after plaques rupture. This review will summarize the connections between hyperlipidemia and TF expression within atherosclerotic plaques and circulating monocytes, as well as its inhibition by statins.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Coronary Artery Disease / blood
  • Coronary Artery Disease / metabolism*
  • Coronary Artery Disease / pathology
  • Humans
  • Lipoproteins, LDL / blood
  • Lipoproteins, LDL / metabolism
  • Plaque, Atherosclerotic / blood
  • Plaque, Atherosclerotic / metabolism*
  • Plaque, Atherosclerotic / pathology
  • Rupture, Spontaneous / blood
  • Rupture, Spontaneous / metabolism
  • Rupture, Spontaneous / pathology
  • Thromboplastin / metabolism*
  • Thrombosis / blood
  • Thrombosis / metabolism*
  • Thrombosis / pathology

Substances

  • Lipoproteins, LDL
  • oxidized low density lipoprotein
  • Thromboplastin