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Mitochondria: diversity in the regulation of the NLRP3 inflammasome
Journal article   Open access   Peer reviewed

Mitochondria: diversity in the regulation of the NLRP3 inflammasome

Prajwal Gurung, John R Lukens and Thirumala-Devi Kanneganti
Trends in molecular medicine, Vol.21(3), pp.193-201
03/2015
DOI: 10.1016/j.molmed.2014.11.008
PMCID: PMC4352396
PMID: 25500014
url
https://doi.org/10.1016/j.molmed.2014.11.008View
Published (Version of record) Open Access

Abstract

•Mitochondrial dysfunction induces specific activation of the NLRP3 inflammasome.•Mitochondria recruit NLRP3 and aid the assembly of the NLRP3 inflammasome.•Autophagy/mitophagy clears damaged mitochondria and induces inflammasome activation.•Mitochondria and NLRP3 dysfunction promotes metabolic diseases. Recent studies have identified new roles for mitochondria in the regulation of autoinflammatory processes. Emerging data suggests that the release of danger signals from mitochondria in response to stress and infection promotes the formation of the inflammatory signaling platform known as inflammasomes. Activation of inflammasomes by damaged mitochondria results in caspase-1-dependent secretion of the inflammatory cytokines interleukin-1β (IL-1β) and IL-18, and an inflammatory form of cell death referred to as pyroptosis. Here, we review recently described mechanisms that have been proposed to be involved in mitochondria-mediated regulation of inflammasome activation and inflammation. In addition, we highlight how aberrant regulation of mitochondria-induced inflammasome activation centrally contributes to the inflammatory process that is responsible for obesity and associated metabolic diseases.
 NLRP3 metabolic disease mitochondria inflammasome

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