Acetaminophen-induced hepatotoxicity in mice is dependent on Tlr9 and the Nalp3 inflammasome.

By Avlin B. Imaeda, Azuma Watanabe, M. Sohail, S. Mahmood, M. Mohamadnejad, F. Sutterwala, R. Flavell, W. Mehal. Journal of Clinical Investigation, 2009

621 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/1019ea1cb133dd835f27612b18422940364ec9a0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. L. Galluzzi
2. Guido Kroemer
3. Oliver Kepp
4. C. Brenner
5. G. Núñez
6. Steven Dooley
7. S. Tait
8. H. Kono

In Molecular Biology

1. Guido Kroemer
2. L. Galluzzi
3. Oliver Kepp
4. E. Latz
5. G. Núñez
6. C. Brenner
7. Grace Y. Chen
8. A. Ramachandran

In Pharmacology

1. L. Galluzzi
2. Guido Kroemer
3. G. Núñez
4. Beth Levine

Citations in the corpus

• Mitochondrial DNA in inflammation and immunity (2020, positive): “TLR9 is crucial for the development of acetaminophen-induced hepatotoxicity [179] and fibrosis [180].”
• Decoding cell death signals in liver inflammation. (2013, background): “Upon binding to TLR9, nuclear DNA released by acetaminophen-exposed hepatocytes promotes the differentiation of hepatic stellate cells (HSCs), hence favoring the secretion of collagen and other fibrosis-associated factors [150], as well as the production of proinflammatory cytokines such as IL-1b an”
• IL-1 receptor antagonist ameliorates inflammasome-dependent alcoholic steatohepatitis in mice. (2012, background): “Emerging data have provided evidence for the role of IL-1 signaling in acute and chronic liver injury of diverse origin, including acetaminophen-induced liver damage (11), nonalcoholic steatohepatitis (12), liver fibrosis (13), and immune-mediated liver injury (14).”
• DAMPening Inflammation by Modulating TLR Signalling (2010, background): “Liver injury DNA During acetaminophen induced cell death induced TLR9 dependent tissue injury [134]”
• Circulating microRNAs in exosomes indicate hepatocyte injury and inflammation in alcoholic, drug-induced and inflammatory liver diseases (2012, background): “Emerging evidence suggests that endogenous danger signals (DAMPs) from dying cells, including DNA, induce sterile inflammation and autoimmunity.(23) Endogenous danger signals such as mitochondrial DNA (TLR9 ligand) are likely to act on the liver in combination with gut-derived endotoxin (TLR4 ligand”
• NLRP3 inflammasome activation results in hepatocyte pyroptosis, liver inflammation and fibrosis (2014, background): “was associated with protection against carbontetrachloride– or thioacetamide-induced liver fibrosis(40) and was found to reduce mortality and liver injury after acetaminophen administration.(41) Future studies to dissect the importance of cell-specific activation of the NLRP3 inflammasome and the ro”
• The sterile inflammatory response (2010, background): “There is also some evidence for a role of TLR3 or TLR9 in sensing cell injury in gut ischemia (55) or in the liver toxicity (38), respectively.”
• Sterile inflammation: sensing and reacting to damage (2010, background): “In the liver, which is normally devoid of microbial exposure, TLR9 has been implicated in triggering cytokine production and hepatocyte toxicity in acetaminophen-induced injur”