Author(s): Brenner DA, Seki E, Taura K, Kisseleva T, Deminicis S,
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Abstract 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. © 2011 The Japan Society of Hepatology.
This article was published in Hepatol Res
and referenced in Journal of Gastrointestinal & Digestive System