Journal
HEPATOLOGY RESEARCH
Volume 41, Issue 7, Pages 683-686Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1872-034X.2011.00814.x
Keywords
fibrosis; Jun N-terminal kinase; liver; reactive oxygen species; Toll-like receptor
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Funding
- Grants-in-Aid for Scientific Research [23390322, 22590728] Funding Source: KAKEN
- NIAAA NIH HHS [R01 AA020172-02, R01 AA020172] Funding Source: Medline
- NIDDK NIH HHS [R01 DK085252, R01 DK085252-01A1, K08 DK081830] Funding Source: Medline
- NIGMS NIH HHS [R01 GM041804] Funding Source: Medline
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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.
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