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Nuclear factor‐κB and the hepatic inflammation‐fibrosis‐cancer axis

Nuclear factor‐κB and the hepatic inflammation‐fibrosis‐cancer axis Nuclear factor‐κB (NF‐κB) is a transcriptional regulator of genes involved in immunity, inflammatory response, cell fate, and function. Recent attention has focused on the pathophysiological role of NF‐κB in the diseased liver. In vivo studies using rodent models of liver disease and cell‐targeted perturbation of NF‐κB activity have revealed complex and multicellular functions in hepatic inflammation, fibrosis, and the development of hepatocellular carcinoma—a process we have termed the “inflammation‐fibrosis‐cancer axis”. This review summarizes the current state of knowledge and provides insight into the vast complexity of the hepatic NF‐κB signaling system, which should provide a rich source of new therapeutic targets. (HEPATOLOGY 2007;46:590–597.) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hepatology Wolters Kluwer Health

Nuclear factor‐κB and the hepatic inflammation‐fibrosis‐cancer axis

Hepatology , Volume 46 (2) – Aug 1, 2007

Nuclear factor‐κB and the hepatic inflammation‐fibrosis‐cancer axis

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References (73)

Publisher
Wolters Kluwer Health
Copyright
Copyright © 2007 American Association for the Study of Liver Diseases
ISSN
0270-9139
eISSN
1527-3350
DOI
10.1002/hep.21802
pmid
17661407
Publisher site
See Article on Publisher Site

Abstract

Nuclear factor‐κB (NF‐κB) is a transcriptional regulator of genes involved in immunity, inflammatory response, cell fate, and function. Recent attention has focused on the pathophysiological role of NF‐κB in the diseased liver. In vivo studies using rodent models of liver disease and cell‐targeted perturbation of NF‐κB activity have revealed complex and multicellular functions in hepatic inflammation, fibrosis, and the development of hepatocellular carcinoma—a process we have termed the “inflammation‐fibrosis‐cancer axis”. This review summarizes the current state of knowledge and provides insight into the vast complexity of the hepatic NF‐κB signaling system, which should provide a rich source of new therapeutic targets. (HEPATOLOGY 2007;46:590–597.)

Journal

HepatologyWolters Kluwer Health

Published: Aug 1, 2007

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