Research Output
Inflammatory Bowel Disease Drugs: A Focus on Autophagy
  Inflammatory bowel disease [IBD] is characterized by chronic inflammation of the gastrointestinal tract. Medications such as corticosteroids, thiopurines, immunomodulators and biologic agents are used to induce and maintain remission; however, response to these drugs is variable and can diminish over time. Defective autophagy has been strongly linked to IBD pathogenesis, with evidence showing that enhancing autophagy may be therapeutically beneficial by regulating inflammation and clearing intestinal pathogens. It is plausible that the therapeutic effects of some IBD drugs are mediated in part through modulation of the autophagy pathway, with studies investigating a wide range of diseases and cell types demonstrating autophagy pathway regulation by these agents.
This review will highlight the current evidence, both in vitro and in vivo, for the modulation of autophagy by drugs routinely used in IBD. A clearer understanding of their mechanisms of action will be invaluable to utilize these drugs in a more targeted and personalized manner in this diverse and often complex group of patients.

  • Type:

    Review

  • Date:

    05 July 2016

  • Publication Status:

    Published

  • Publisher

    Oxford University Press (OUP)

  • DOI:

    10.1093/ecco-jcc/jjw127

  • Cross Ref:

    10.1093/ecco-jcc/jjw127

  • ISSN:

    1873-9946

  • Library of Congress:

    RC Internal medicine

  • Dewey Decimal Classification:

    616 Diseases

Citation

Hooper, K. M., Barlow, P. G., Stevens, C., & Henderson, P. (2017). Inflammatory Bowel Disease Drugs: A Focus on Autophagy. Journal of Crohn's and Colitis, 11(1), 118-127. https://doi.org/10.1093/ecco-jcc/jjw127

Authors

Keywords

Autophagy, drugs, IBD, Crohn's disease,

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    Inflammatory Bowel Disease Drugs: A Focus on Autophagy

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    © European Crohn’s and Colitis Organistion (ECCO) 2016. 1
    Journal of Crohn's and Colitis, 2016, 1–10
    doi:10.1093/ecco-jcc/jjw127
    Review Article
    This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License
    (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium,
    provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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