Targeting hypoxia in inflammatory bowel disease

J Investig Med. 2016 Feb;64(2):364-8. doi: 10.1097/JIM.0000000000000218. Epub 2016 Jan 11.

Abstract

In this review, I summarize some of the recent insight into pharmacological targeting of hypoxia in disease models. Studies from cultured cell systems, animal models, and translation to human patients have revealed that posttranslational modifications of individual proteins within NF-κB and hypoxia-inducible factor pathways serve as ideal targets for analysis in disease models. Studies defining differences and similarities between these responses have taught us a number of important lessons about the complexity of the inflammatory response. A clearer definition of these pathways has provided new insight into disease pathogenesis and, importantly, the potential for new therapeutic targets.

Keywords: epithelia; hypoxia; inflammation; mucosa; transcription; translation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Humans
  • Hydroxylation
  • Hypoxia / complications*
  • Hypoxia / pathology*
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Inflammatory Bowel Diseases / complications*
  • Inflammatory Bowel Diseases / pathology*
  • Intestinal Mucosa / pathology
  • Protein Processing, Post-Translational

Substances

  • Hypoxia-Inducible Factor 1, alpha Subunit