Interdependent roles for hypoxia inducible factor and nuclear factor-kappaB in hypoxic inflammation.

  • Taylor C
  • 97


    Mendeley users who have this article in their library.
  • N/A


    Citations of this article.


Decreased oxygen availability (hypoxia) is a hallmark feature of the microenvironment in a number of chronic inflammatory conditions including arthritis and inflammatory bowel disease (IBD). Recent advances in our understanding of oxygen-dependent cell signalling have uncovered several mechanisms by which hypoxia impacts upon the development of inflammation through the coordinated expression of adaptive, inflammatory and apoptotic genes. Two central transcription factors involved in the regulation of this response are hypoxia inducible factor (HIF) and nuclear factor-kappaB (NF-kappaB) which display different degrees of sensitivity to activation during hypoxia. Furthermore, HIF and NF-kappaB demonstrate an intimate interdependence at several mechanistic levels. Recent studies indicate that these pathways may represent important new therapeutic targets in diseases characterized by hypoxic inflammation.

Author-supplied keywords

  • Animals
  • Anoxia
  • Anoxia: metabolism
  • Humans
  • Hypoxia-Inducible Factor 1
  • Hypoxia-Inducible Factor 1: metabolism
  • Inflammation
  • Inflammation: metabolism
  • Mice
  • NF-kappa B
  • NF-kappa B: metabolism

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document


  • Cormac T Taylor

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free