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

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Affiliations

  • 1. Christian Doppler Research Laboratory for Gut Inflammation, Medical University Innsbruck, Innsbruck, Austria.
      Authors
    • Tilg H 1
    (1 author)

ORCIDs linked to this article

Hepatology (Baltimore, Md.), 01 Nov 2010, 52(5):1836-1846
https://doi.org/10.1002/hep.24001 PMID: 21038418 

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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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