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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 PLoS+One
2017 ; 12
(3
): e0172575
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
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
): e0172575
PMID28249038
show 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.