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This Article Full Text Full Text (PDF) All Versions of this Article: 586/17/4055    most recent jphysiol.2008.157669v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Taylor, C. T. PubMed PubMed Citation Articles by Taylor, C. T. Related Collections Review articles Cellular

¹ UCD Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland

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-B (NF-B) which display different degrees of sensitivity to activation during hypoxia. Furthermore, HIF and NF-B 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.

(Received 3 June 2008; accepted after revision 3 July 2008; first published online 3 July 2008)
Corresponding author C. T. Taylor: UCD Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland. Email: cormac.taylor{at}ucd.ie