1. Nuclear Factor-κB in the Liver: Friend or Foe?
Robert F. Schwabe, David A. Brenner 
Gastroenterology 
Volume 132, Issue 7, Pages (June 2007)
DOI: /j.gastro
Copyright © 2007 AGA Institute Terms and Conditions

2. Figure 1
Role of p65 and NEMO in hepatocyte death. In hepatocytes, TNFα activates NF-κB to inhibit the activation of concurrent proapoptotic pathways such JNK and executioner caspases. Hepatocyte specific inactivation of NEMO or p65 completely prevents TNFα-induced NF-κB activation in hepatocytes leading to massive activation of JNK and caspases, and cell death. During hepatic ischemia-reperfusion (“IR”), an increase in hepatocyte cell death promotes Kupffer cells infiltration and activation, and Kupffer cell-mediated TNFα release. Hepatocytes with a complete absence of NF-κB activation due to inactivation of NEMO show an increased rate of apoptosis in response to the increased TNFα levels and may start a vicious cycle in which dead hepatocytes further contribute to Kupffer cell activation, rising TNFα levels and a next round of hepatocyte cell death.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2007 AGA Institute Terms and Conditions