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The rOX-stars of inflammation: links between the inflammasome and mitochondrial meltdown

Caroline L Holley1, Kate Schroder1

  • 1Institute for Molecular Bioscience IMB Centre for Inflammation and Disease Research The University of Queensland St. Lucia QLD Australia.

Clinical & Translational Immunology
|February 15, 2020
PubMed

Insights

Mitochondrial dysfunction triggers inflammation by activating the NLRP3 inflammasome. Understanding mitochondria

Area of Science:

  • Immunology
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Mitochondria, essential for cellular energy, harbor molecules that trigger innate immunity.
  • Mitochondrial damage from various factors can cause persistent inflammasome signaling, leading to inflammation.

Purpose of the Study:

  • To review how mitochondria activate the NLRP3 inflammasome.
  • To explore the link between mitochondrial features and inflammatory signaling.

Main Methods:

  • Literature review focusing on mitochondrial dysfunction and NLRP3 inflammasome activation.
  • Analysis of the interplay between mitochondrial dynamics, metabolism, redox state, and inflammasome activity.

Main Results:

  • Mitochondria act as a source of danger signals that activate the NLRP3 inflammasome.
  • Persistent mitochondrial damage leads to sustained and inappropriate inflammasome activation.

Conclusions:

  • Mitochondrial features directly drive inflammatory signaling via the NLRP3 inflammasome.
  • A holistic approach is crucial for studying NLRP3 activation by dysfunctional mitochondria, considering interconnected mitochondrial functions.
Keywords:
NLRP3ROSinfectioninflammasomemitochondria

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