Oxidative risk for atherothrombotic cardiovascular disease

Free Radic Biol Med. 2009 Dec 15;47(12):1673-706. doi: 10.1016/j.freeradbiomed.2009.09.009. Epub 2009 Sep 12.

Abstract

In the vasculature, reactive oxidant species, including reactive oxygen, nitrogen, or halogenating species, and thiyl, tyrosyl, or protein radicals may oxidatively modify lipids and proteins with deleterious consequences for vascular function. These biologically active free radical and nonradical species may be produced by increased activation of oxidant-generating sources and/or decreased cellular antioxidant capacity. Once formed, these species may engage in reactions to yield more potent oxidants that promote transition of the homeostatic vascular phenotype to a pathobiological state that is permissive for atherothrombogenesis. This dysfunctional vasculature is characterized by lipid peroxidation and aberrant lipid deposition, inflammation, immune cell activation, platelet activation, thrombus formation, and disturbed hemodynamic flow. Each of these pathobiological states is associated with an increase in the vascular burden of free radical species-derived oxidation products and, thereby, implicates increased oxidant stress in the pathogenesis of atherothrombotic vascular disease.

Publication types

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

MeSH terms

  • Cardiovascular Diseases / etiology*
  • Cardiovascular Diseases / metabolism
  • Free Radicals / metabolism*
  • Humans
  • Lipid Peroxidation
  • Oxidative Stress*
  • Oxidoreductases / metabolism*
  • Thrombosis / etiology*
  • Thrombosis / metabolism

Substances

  • Free Radicals
  • Oxidoreductases