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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
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The NRF2/Keap1 pathway as a therapeutic target in inflammatory bowel disease

Sem Geertsema1, Arno R Bourgonje2, Raphael R Fagundes1

  • 1Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

Trends in Molecular Medicine
|August 9, 2023
PubMed

Insights

This review examines the NRF2/Keap1 pathway

Area of Science:

  • Gastroenterology and Immunology
  • Molecular Biology
  • Drug Discovery

Background:

  • Oxidative stress (OS) is a key factor in inflammatory bowel disease (IBD) pathogenesis.
  • Previous clinical trials targeting OS in IBD have shown inconsistent outcomes.
  • The NRF2/Keap1 pathway regulates cellular antioxidant defenses and is implicated in IBD.

Purpose of the Study:

  • To review human evidence on modulating the NRF2/Keap1 pathway in IBD.
  • To explore the NRF2/Keap1 pathway as a therapeutic target for IBD.
  • To present compounds that activate this pathway for potential clinical use.

Main Methods:

  • Literature review of studies investigating the NRF2/Keap1 pathway in IBD.
  • Analysis of existing human data on NRF2/Keap1 modulation.
  • Identification and summary of compounds targeting the NRF2/Keap1 axis.

Main Results:

  • Dysregulation of the NRF2/Keap1 pathway is observed in IBD.
  • Activation of NRF2/Keap1 may enhance antioxidant responses, potentially mitigating IBD.
  • Evidence for direct clinical modulation of NRF2/Keap1 in IBD is currently limited.

Conclusions:

  • The NRF2/Keap1 pathway represents a promising therapeutic target for IBD.
  • Further research and clinical trials are needed to validate compounds targeting this pathway.
  • Modulating NRF2/Keap1 offers a potential strategy to improve IBD treatment outcomes.
Keywords:
NRF2/Keap1 pathwayinflammatory bowel diseaseoxidative stresspersonalized medicineredox medicine

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