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      Evolution of inflammation in nonalcoholic fatty liver disease: the multiple parallel hits hypothesis.

      1 ,
      Hepatology (Baltimore, Md.)
      Wiley

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          Abstract

          Whereas in most cases a fatty liver remains free of inflammation, 10%-20% of patients who have fatty liver develop inflammation and fibrosis (nonalcoholic steatohepatitis [NASH]). Inflammation may precede steatosis in certain instances. Therefore, NASH could reflect a disease where inflammation is followed by steatosis. In contrast, NASH subsequent to simple steatosis may be the consequence of a failure of antilipotoxic protection. In both situations, many parallel hits derived from the gut and/or the adipose tissue may promote liver inflammation. Endoplasmic reticulum stress and related signaling networks, (adipo)cytokines, and innate immunity are emerging as central pathways that regulate key features of NASH.

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          Author and article information

          Journal
          Hepatology
          Hepatology (Baltimore, Md.)
          Wiley
          1527-3350
          0270-9139
          Nov 2010
          : 52
          : 5
          Affiliations
          [1 ] Christian Doppler Research Laboratory for Gut Inflammation, Medical University Innsbruck, Innsbruck, Austria. herbert.tilg@i-med.ac.at
          Article
          10.1002/hep.24001
          21038418
          15f386b0-3943-4896-9f2e-1a8f6c82ad01
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