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10.1371/journal.pone.0172575

http://scihub22266oqcxt.onion/10.1371/journal.pone.0172575
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C5331985!5331985!28249038
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suck abstract from ncbi


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pmid28249038      PLoS+One 2017 ; 12 (3): �
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  • Microvesicles released from fat-laden cells promote activation of hepatocellular NLRP3 inflammasome: A pro-inflammatory link between lipotoxicity and non-alcoholic steatohepatitis #MMPMID28249038
  • Cannito S; Morello E; Bocca C; Foglia B; Benetti E; Novo E; Chiazza F; Rogazzo M; Fantozzi R; Povero D; Sutti S; Bugianesi E; Feldstein AE; Albano E; Collino M; Parola M
  • PLoS One 2017[]; 12 (3): � PMID28249038show ga
  • Non-Alcoholic Fatty Liver Disease (NAFLD) is a major form of chronic liver disease in the general population in relation to its high prevalence among overweight/obese individuals and patients with diabetes type II or metabolic syndrome. NAFLD can progress to steatohepatitis (NASH), fibrosis and cirrhosis and end-stage of liver disease but mechanisms involved are still incompletely characterized. Within the mechanisms proposed to mediate the progression of NAFLD, lipotoxicity is believed to play a major role. In the present study we provide data suggesting that microvesicles (MVs) released by fat-laden cells undergoing lipotoxicity can activate NLRP3 inflammasome following internalization by either cells of hepatocellular origin or macrophages. Inflammasome activation involves NF-kB-mediated up-regulation of NLRP3, pro-caspase-1 and pro-Interleukin-1, then inflammasome complex formation and Caspase-1 activation leading finally to an increased release of IL-1?. Since the release of MVs from lipotoxic cells and the activation of NLRP3 inflammasome have been reported to occur in vivo in either clinical or experimental NASH, these data suggest a novel rational link between lipotoxicity and increased inflammatory response.



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