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Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis
Author(s) -
Tilg Herbert,
Moschen Alexander R.
Publication year - 2010
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.24001
Subject(s) - inflammation , steatosis , nonalcoholic fatty liver disease , steatohepatitis , fatty liver , fibrosis , nonalcoholic steatohepatitis , adipose tissue , endoplasmic reticulum , medicine , biology , immunology , disease , pathology , microbiology and biotechnology
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. (HEPATOLOGY 2010;52:1836‐1846)