The NLRP3 inflammasome - interleukin 1 pathway as a therapeutic target in gout

Zoltán Szekanecz, Szilvia Szamosi, Gergő E. Kovács, Elek Kocsis, Szilvia Benkő

Research output: Contribution to journalReview article

5 Citations (Scopus)


The NLRP3 inflammasome is implicated in the processing of the pro-inflammatory cytokine interleukin 1β. Inflammatory disorders associated with the activation of the NLRP3 inflammasome - IL-1 axis are termed autoinflammatory diseases. Gout is an autoinflammatory disease, which is triggered by the deposition of monosodium urate crystals of precipitated uric acid. It is characterized by recurrent attacks of inflammation due to the activation of phagocytic cells that try to clear the crystals. NLRP3 inflammasome-mediated IL-1β production plays a key role in the manifestation of the disease. Currently, the best approach to treat gout is to reduce uric acid concentration by targeting xanthine oxidase or uric acid transporters, or to use non-steroidal anti-inflammatory drugs. Nevertheless, most of these treatments are not effective enough and may results in side effects. During the past decades, our knowledge has greatly improved about the molecular mechanisms of NLRP3 activation. This knowledge enables and urges scientists to discover or design drugs that target pathways of NLRP3 inflammasome activation, or more preferentially, NLRP3 inflammasome itself. In this review, we discuss the already available drugs and products, that target the diverse pathways of the NLRP3 - IL-1β axis, and the future therapeutic perspectives.

Original languageEnglish
Pages (from-to)82-93
Number of pages12
JournalArchives of Biochemistry and Biophysics
Publication statusPublished - Jul 30 2019


  • Autoinflammatory disease
  • Gout
  • Inflammasome
  • Interleukin 1
  • NLRP3

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology

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