cell signals influencing hepatic fibrosis影响肝纤维化细胞信号.pdfVIP

Hindawi Publishing Corporation International Journal of Hepatology Volume 2012, Article ID 158547, 18 pages doi:10.1155/2012/158547 Review Article Cell Signals Influencing Hepatic Fibrosis Min Cong, Keiko Iwaisako, Chunyan Jiang, and Tatiana Kisseleva Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA Correspondence should be addressed to Tatiana Kisseleva, tkisseleva@ Received 1 March 2012; Accepted 1 June 2012 Academic Editor: Michael Ott Copyright © 2012 Min Cong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Liver fibrosis is the result of the entire organism responding to a chronic injury. Every cell type in the liver contributes to the fibrosis. This paper first discusses key intracellular signaling pathways that are induced during liver fibrosis. The paper then examines the effects of these signaling pathways on the major cell types in the liver. This will provide insights into the molecular pathophysiology of liver fibrosis and should identify therapeutic targets. 1. Introduction retain a quiescent phenotype (qHSCs), but following TGF- β 1 stimulation, PDGF, or matrix stiffness, or other fibrogenic Fibrosis is the outcome of many chronic liver diseases [1], stimuli they rapidly activate into type I collagen, α-smooth including hepatitis B virus (HBV), hepatitis C virus (HCV), muscle actin expressing myofibroblasts (aHSCs) [ 1, 4, 6]. In alcoholic liver disease, and nonalcoholic steatohepatitis addition to HSCs,