Transcription factor and kinase-mediated signaling in atherosclerosis and vascular injury

Curr Atheroscler Rep. 2006 May;8(3):252-60. doi: 10.1007/s11883-006-0081-1.


Our understanding of the molecular signaling pathways regulating the initiation and progression of atherosclerosis or remodeling in response to injury has begun to cross the boundaries from regulation of well-described canonical pathways to the interplay between these pathways. The focus of this review is to summarize our current understanding of a finite group of transcription factors and kinases involved in vascular injury and atherosclerosis, including nuclear factor-kappaB (NF-kappaB), early growth response factor-1 (Egr-1), activator protein-1 (AP-1), hypoxia inducible factor-1alpha (HIF-1alpha), homeobox, and T cell factor/lymphoid enhancer factor (Tcf-Lef), as well as the kinases janus kinase/signal transducers and activators of transcription (JAK/STAT), protein kinase C (PKC), p38, Rho, ERK5, JNK, p44/p42, and phosphoinositide 3 (PI3) kinase/AKT.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis / enzymology*
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Models, Biological
  • NF-kappa B / metabolism
  • Phosphotransferases / physiology*
  • Signal Transduction
  • Transcription Factors / physiology*
  • Transcription, Genetic
  • Vascular Diseases / enzymology*
  • Vascular Diseases / pathology


  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • NF-kappa B
  • Transcription Factors
  • Phosphotransferases