Inflammation meets oxidation: NF-kappaB as a mediator of initial lesion development in atherosclerosis

Trends Mol Med. 2003 Dec;9(12):549-57. doi: 10.1016/j.molmed.2003.10.007.


Transcription factor nuclear factor-kappaB (NF-kappaB) and its target genes are involved in the pathogenesis of atherosclerosis, in addition to many other diseases. Monocyte recruitment into subendothelial space is primarily mediated by NF-kappaB-dependent gene expression, and this event is a crucial milestone, because it is nearly impossible to reverse the progression of the lesion after this point. Recent advances in our understanding of atherosclerosis as a disease of childhood enforces the necessity of developing novel approaches for prevention and treatment. Here, the authors address NF-kappaB as a major therapeutic target, especially for preventive measures, in the light of two main hypotheses of atherosclerosis: oxidation and inflammation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Arteriosclerosis / metabolism*
  • Arteriosclerosis / pathology
  • Cell Adhesion
  • Humans
  • Inflammation*
  • Models, Biological
  • NF-kappa B / metabolism
  • NF-kappa B / physiology*
  • Oxygen / metabolism*


  • NF-kappa B
  • Oxygen