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Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Hepatol 2017 ; 66 (4): 836-48 Nephropedia Template TP
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Role of the Inflammasome in Acetaminophen-induced Liver Injury and Acute Liver Failure #MMPMID27913221
Woolbright BL; Jaeschke H
J Hepatol 2017[Apr]; 66 (4): 836-48 PMID27913221show ga
Drug-induced acute liver failure carries a high morbidity and mortality rate. Acetaminophen overdose is the number one cause of acute liver failure and remains a major problem in Western medicine. Administration of N-acetyl cysteine is an effective antidote when given before the initial rise in toxicity; however, many patients present to the hospital after this stage occurs. As such, treatments which can alleviate late-stage acetaminophen-induced acute liver failure are imperative. While the initial mechanisms of toxicity are well described, a debate has occurred recently in the literature over whether or not there exists a second phase of injury, mediated by inflammatory processes. Critical to this potential inflammatory process is the activation of caspase-1 and interleukin-1ß by a molecular complex known as the inflammasome. A number of different stimuli for formation of multiple different inflammasome complexes have been identified. Formation of the Nalp3 inflammasome in particular has directly been attributed to late-stage acetaminophen toxicity. In this review, we will discuss mechanisms of acetaminophen-induced liver injury in mice and man with a particular focus on the role of inflammation and the inflammasome.