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Gastroenterology Research and PracticeVolume 2010 2010, Article ID 598109, 7 pages

Review ArticleDepartment of Surgery, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan

Received 24 March 2010; Accepted 28 August 2010

Academic Editor: Ekihiro Seki

Copyright © 2010 Yuji Iimuro and Jiro Fujimoto. 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.


While hepatocytes rarely undergo proliferation in normal livers, they quickly induce proliferation in response to loss of liver mass by toxin or inflammation-induced hepatocyte injury, trauma, or surgical resection, leading to a restoration of liver mass to its original size. Recent studies suggest that Toll-like receptor TLR signaling participates in this regenerative response. Myeloid differentiation factor MyD88, a common adaptor molecule in the TLR, IL-1 and IL-18 receptor signaling, plays a key role, at least, in the early phase of liver regeneration. Currently, definite ligands which bind to TLRs and initiate this process are still unclear. TLRs stimulated by their corresponding ligands, as well as tumor necrosis factor TNF receptors TNFRs, can activate downstream signal molecules, including transcription factor nuclear factor NF- B and c-Jun N-terminal kinase JNK. Previous studies have revealed the important role of TNF receptor signaling, NF- B, and JNK in liver regeneration by using hepatocyte-specific gene-modified animals. This review will summarize the current knowledge of TLR signaling and their related molecules in liver regeneration. We will also discuss whether modulating these factors may become new therapeutic strategies to promote liver regeneration in various clinical situations.

Author: Yuji Iimuro and Jiro Fujimoto



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