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The most recent version of this article was published on 1 February 2008

Gut. Published Online First: 3 August 2007. doi:10.1136/gut.2007.124115
Copyright © 2007 BMJ Publishing Group Ltd & British Society of Gastroenterology.

Paper

The Role of NF-{kappa}B Activation in the Pathogenesis of Acute Pancreatitis

Zoltan Rakonczay Jr.1*, Peter Hegyi 1, Tamas Takacs 1, Joshua McCarroll 2 and Ashok Saluja 3

1 University of Szeged, Hungary
2 Children's Cancer Institute Australia for Medical Research, Australia
3 University of Minnesota, United States

* To whom correspondence should be addressed. E-mail: raz{at}in1st.szote.u-szeged.hu.

Accepted 17 July 2007


Abstract

Acute pancreatitis is an inflammatory disease of the pancreas which, in its most severe form, is associated with multiorgan failure and death. Recently, signaling molecules and pathways which are responsible for the initiation and progression of this disease have been under intense scrutiny. One important signaling molecule, nuclear factor {kappa}B (NF-{kappa}B), has been shown to play an important role in the development of acute pancreatitis. NF-{kappa}B is a nuclear transcription factor which plays a critical role in regulating the transcription of a wide variety of genes involved in immunity and inflammation. Many of these genes have been implicated as central players in the development and progression of acute pancreatitis. This review discusses recent advances in the investigation of pancreatic and extrapancreatic (lungs, liver, monocytes and macrophages, and endothelial cells) NF-{kappa}B activation as it relates to acute pancreatitis.

Keywords: NF-kB, acute pancreatitis


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This article has been cited by other articles:

  • Binker, M. G., Binker-Cosen, A. A., Gaisano, H. Y., Cosen-Binker, L. I. (2008). Inhibition of Rac1 decreases the severity of pancreatitis and pancreatitis-associated lung injury in mice. Exp Physiol 93: 1091-1103 [Abstract] [Full Text]  

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