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Non‐alcoholic steatohepatitis‐induced fibrosis: Toll‐like receptors, reactive oxygen species and Jun N‐terminal kinase
Author(s) -
Brenner David A.,
Seki Ekihiro,
Taura Kojiro,
Kisseleva Tatiana,
Deminicis Samuele,
Iwaisako Keiko,
Inokuchi Sayaka,
Schnabl Bernd,
Oesterreicher Christopher H.,
Paik Yong H.,
Miura Kouichi,
Kodama Yuzo
Publication year - 2011
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2011.00814.x
Subject(s) - steatohepatitis , fibrosis , cirrhosis , steatosis , fatty liver , cancer research , toll like receptor , receptor , signal transduction , reactive oxygen species , hepatic fibrosis , microbiology and biotechnology , medicine , chemistry , biology , innate immune system , disease
Non‐alcoholic steatohepatitis (NASH) represents the progression of hepatic steatosis to streatohepatitis, fibrosis and cirrhosis. Three signaling pathways have been associated with this progression; Toll‐like receptors, reactive oxygen species and Jun N‐terminal kinase. This review will describe how activation of these three pathways is required for development of fibrosis in murine models of NASH. The three pathways are related and synergistic through intracellular cross‐talk. Disruption of any of these pathways may inhibit NASH‐induced fibrosis and are potential targets for therapeutic intervention.