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10.1016/j.it.2014.02.007

http://scihub22266oqcxt.onion/10.1016/j.it.2014.02.007
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C4041823!4041823!24646829
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suck abstract from ncbi


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pmid24646829      Trends+Immunol 2014 ; 35 (6): 253-61
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  • Calcuim signaling and mitochondrial destabilization in the triggering of the NLRP3 inflammasome #MMPMID24646829
  • Horng T
  • Trends Immunol 2014[Jun]; 35 (6): 253-61 PMID24646829show ga
  • The NLRP3 inflammasome is a cytosolic complex that activates Caspase-1, leading to maturation of IL-1? and IL-18 and induction of a pro-inflammatory cell death in sentinel cells of the innate immune system. Diverse stimuli have been shown to activate the NLRP3 inflammasome during infection and metabolic diseases, thus implicating the pathway in triggering both adaptive and maladaptive inflammation in a variety of clinically important settings. Here I discuss the emerging model that signals associated with mitochondrial destabilization may critically activate the NLRP3 inflammasome. Together with studies indicating an important role for Ca2+ signaling, these findings suggest that many stimuli engage Ca2+ signaling as an intermediate step to trigger mitochondrial destabilization, thus generating the mitochondria-associated ligands that activate the NLRP3 inflammasome.
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