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The Crosstalk between Nrf2 and Inflammasomes.

Paulina Hennig1, Martha Garstkiewicz2, Serena Grossi3

  • 1Department of Dermatology, University Hospital of Zurich, Gloriastrasse 31, F30, CH-8091 Zurich, Switzerland. Paulina.Hennig@usz.ch.

International Journal of Molecular Sciences
|February 14, 2018
PubMed
Summary

The Nrf2 pathway, a cellular defense mechanism, and inflammasomes, regulators of inflammation, have an antagonistic relationship. Nrf2 activation inhibits inflammasomes, thereby reducing inflammation and cell death.

Keywords:
Nrf2caspase-1inflammasomeinflammationnucleotide-binding oligomerization domain (NOD)-like receptor containing pyrin domain 3 (NLRP3)

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Immunology

Background:

  • The Nrf2 (nuclear factor E2-related factor or nuclear factor (erythroid-derived 2)-like 2) transcription factor is crucial for cytoprotection against oxidative stress.
  • Inflammasomes are key regulators of inflammation, mediating the secretion of proinflammatory cytokines and pyroptosis (inflammatory cell death).

Purpose of the Study:

  • To review the complex interplay between the Nrf2 and inflammasome pathways.
  • To elucidate the predominantly antagonistic relationship between these two stress-activated pathways.

Main Methods:

  • Literature review of studies investigating Nrf2 and inflammasome signaling.
  • Analysis of experimental evidence demonstrating the crosstalk between Nrf2 and inflammasomes.

Main Results:

  • Nrf2 activation is linked to the inhibition of inflammasome assembly and activation.
  • Nrf2-activating compounds have been shown to suppress inflammasome-mediated inflammation and pyroptosis.

Conclusions:

  • The Nrf2 and inflammasome pathways exhibit a significant, largely antagonistic crosstalk.
  • Modulating the Nrf2 pathway offers a potential therapeutic strategy to control inflammation.