Evolution of inflammation in nonalcoholic fatty liver disease: the multiple parallel hits hypothesis - PubMed (original) (raw)

Review

. 2010 Nov;52(5):1836-46.

doi: 10.1002/hep.24001.

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• PMID: 21038418
• DOI: 10.1002/hep.24001

Review

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

Herbert Tilg et al. Hepatology. 2010 Nov.

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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