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10.1016/j.molmed.2014.11.008

http://scihub22266oqcxt.onion/10.1016/j.molmed.2014.11.008
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C4352396!4352396!25500014
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suck abstract from ncbi


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pmid25500014      Trends+Mol+Med 2015 ; 21 (3): 193-201
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  • Mitochondria: Diversity in the regulation of NLRP3 inflammasome #MMPMID25500014
  • Gurung P; Lukens JR; Kanneganti TD
  • Trends Mol Med 2015[Mar]; 21 (3): 193-201 PMID25500014show ga
  • 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 IL-1? 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 are responsible for obesity and associated metabolic diseases.
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