| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3293949 | Gastroenterology | 2010 | 19 Pages |
Abstract
In a mouse model of NASH, TLR9 signaling induces production of IL-1β by Kupffer cells, leading to steatosis, inflammation, and fibrosis.
Keywords
IL-1RCpGIL-1βIκBODNoligodeoxynucleotideTLRNIHMCDHSCPAI-1CDAADGAT2TIMP1NAFLDcytosine phosphate guanineCSAANF-κBHOMA-IRALTTNFαTGFβBacterial DNAAdenosine TriphosphateATPalanine transaminasehomeostasis model assessment of insulin resistancenonalcoholic steatohepatitisInterleukin-1βtissue inhibitor of metalloproteinase-1Bambinon-alcoholic fatty liver diseaseTransforming growth factor βtumor necrosis factor αTUNELToll-like receptordiacylglycerol acyltransferase 2Hepatic stellate cellIRAK-Mnuclear factor-κBlactate dehydrogenaseLDHNIH, National Institutes of Healthmethionine and choline deficientPlasminogen activator inhibitor-1inhibitor of NF-κBNash wild-typepolymerase chain reactionPCRinterleukin-1 receptorToll-like receptors
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Authors
Kouichi Miura, Yuzo Kodama, Sayaka Inokuchi, Bernd Schnabl, Tomonori Aoyama, Hirohide Ohnishi, Jerrold M. Olefsky, David A. Brenner, Ekihiro Seki,