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Mitochondria: diversity in the regulation of the NLRP3 inflammasome

Prajwal Gurung1, John R Lukens2, Thirumala-Devi Kanneganti1

  • 1Department of Immunology, St Jude Children's Research Hospital, Memphis, TN 38105, USA.

Trends in Molecular Medicine
|December 16, 2014
PubMed

Insights

Mitochondria danger signals activate inflammasomes, leading to inflammation and cell death. Dysregulation contributes to metabolic diseases like obesity.

Area of Science:

  • Mitochondrial biology
  • Immunology
  • Metabolic disease research

Background:

  • Mitochondria play a newly identified role in regulating autoinflammatory processes.
  • Mitochondrial danger signals released during stress or infection activate inflammasomes.

Purpose of the Study:

  • To review mechanisms of mitochondria-mediated inflammasome activation.
  • To highlight the role of mitochondrial inflammasome dysregulation in metabolic diseases.

Main Methods:

  • Literature review of recent studies on mitochondria and inflammation.
  • Analysis of proposed mechanisms linking mitochondria to inflammasome activation.

Main Results:

  • Mitochondrial damage triggers inflammasome assembly and activation.
  • Activated inflammasomes lead to IL-1β and IL-18 secretion and pyroptosis.
  • Aberrant mitochondrial regulation of inflammasomes is implicated in obesity and metabolic dysfunction.

Conclusions:

  • Mitochondria are key regulators of inflammasome-driven inflammation.
  • Mitochondrial dysfunction contributes significantly to the pathogenesis of obesity and metabolic diseases.
Keywords:
NLRP3inflammasomemetabolic diseasemitochondria

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