[HTML][HTML] Mitochondria: diversity in the regulation of the NLRP3 inflammasome

P Gurung, JR Lukens, TD Kanneganti - Trends in molecular medicine, 2015 - cell.com
Trends in molecular medicine, 2015cell.com
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 …
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.
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