Non-alcoholic steatohepatitis-induced fibrosis: Toll-like receptors, reactive oxygen species and Jun N-terminal kinase

被引：40

作者：

Brenner, David A. ^{[1
]}

Seki, Ekihiro ^{[1
]}

Taura, Kojiro ^{[1
]}

Kisseleva, Tatiana ^{[1
]}

Deminicis, Samuele ^{[1
]}

Iwaisako, Keiko ^{[1
]}

Inokuchi, Sayaka ^{[1
]}

Schnabl, Bernd ^{[1
]}

Oesterreicher, Christopher H. ^{[1
]}

Paik, Yong H. ^{[1
]}

Miura, Kouichi ^{[1
]}

Kodama, Yuzo ^{[1
]}

机构：

[1] UC San Diego Hlth Sci, Dept Med, La Jolla, CA 92093 USA

来源：

HEPATOLOGY RESEARCH | 2011年 / 41卷 / 07期

关键词：

fibrosis; Jun N-terminal kinase; liver; reactive oxygen species; Toll-like receptor;

D O I：

10.1111/j.1872-034X.2011.00814.x

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

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.

引用

页码：683 / 686

页数：4

共 3 条

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