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Am J Physiol Gastrointest Liver Physiol 284: G875-G879, 2003; doi:10.1152/ajpgi.00549.2002
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Vol. 284, Issue 6, G875-G879, June 2003

THEME
The Future of GI and Liver Research: Editorial Perspectives
III. JNK/AP-1 regulation of hepatocyte death

Mark J. Czaja

Marion Bessin Liver Research Center and Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461

Activation of the JNK/activator protein-1 (AP-1)-signaling pathway is a common mediator of hepatocyte death from a variety of stimuli. Although the mechanism by which JNK or AP-1 promotes death is unknown, it results when activation of this signaling pathway is unusually prolonged. Although JNK/AP-1 mediates TNF-induced cell death at or above the level of the mitochondria, the ability of JNK/AP-1 to promote death from necrosis as well as apoptosis suggests that JNK/AP-1 may induce death by several mechanisms. Recognition of JNK/AP-1 signaling as a critical promoter of hepatocyte death raises the possibility that the therapeutic manipulation of this pathway may be effective in the treatment of human liver disease.

mitogen-activated protein kinase; hepatocyte; c-Jun; apoptosis; tumor necrosis factor


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