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Toll-like receptor 4 signaling in liver injury and hepatic fibrogenesis

Authors
  • Guo, Jinsheng1
  • Friedman, Scott L2
  • 1 Fu Dan University, Division of Digestive Diseases, Zhong Shan Hospital, Department of Internal Medicine, Shanghai Medical College, Shanghai, China , Shanghai (China)
  • 2 Mount Sinai Hospital, Mount Sinai School of Medicine, Division of Liver Diseases, New York, NY, USA , New York (United States)
Type
Published Article
Journal
Fibrogenesis & Tissue Repair
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Oct 21, 2010
Volume
3
Issue
1
Identifiers
DOI: 10.1186/1755-1536-3-21
Source
Springer Nature
Keywords
License
Green

Abstract

Toll-like receptors (TLRs) are a family of transmembrane pattern recognition receptors (PRR) that play a key role in innate and adaptive immunity by recognizing structural components unique to bacteria, fungi and viruses. TLR4 is the most studied of the TLRs, and its primary exogenous ligand is lipopolysaccharide, a component of Gram-negative bacterial walls. In the absence of exogenous microbes, endogenous ligands including damage-associated molecular pattern molecules from damaged matrix and injured cells can also activate TLR4 signaling. In humans, single nucleotide polymorphisms of the TLR4 gene have an effect on its signal transduction and on associated risks of specific diseases, including cirrhosis. In liver, TLR4 is expressed by all parenchymal and non-parenchymal cell types, and contributes to tissue damage caused by a variety of etiologies. Intact TLR4 signaling was identified in hepatic stellate cells (HSCs), the major fibrogenic cell type in injured liver, and mediates key responses including an inflammatory phenotype, fibrogenesis and anti-apoptotic properties. Further clarification of the function and endogenous ligands of TLR4 signaling in HSCs and other liver cells could uncover novel mechanisms of fibrogenesis and facilitate the development of therapeutic strategies.

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