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AMPK-associated signaling to bridge the gap between fuel metabolism and hepatocyte viability

Cited 33 time in Web of Science Cited 34 time in Scopus
Authors
Yang, Yoon Mee; Han, Chang Yeob; Kim, Yoon Jun; Kim, Sang Geon
Issue Date
2010-08-14
Publisher
W J G PRESS
Citation
WORLD JOURNAL OF GASTROENTEROLOGY; Vol.16 30; 3731-3742
Keywords
Adenosine monophosphate-activated protein kinaseCell survivalFatty liverp70 ribosomal S6 kinase-1Glycogen synthase kinase 3 betaInsulin resistanceEnergy metabolism
Abstract
The adenosine monophosphate-activated protein kinase (AMPK) and p70 ribosomal S6 kinase-1 pathway may serve as a key signaling flow that regulates energy metabolism; thus, this pathway becomes an attractive target for the treatment of liver diseases that result from metabolic derangements. In addition, AMPK emerges as a kinase that controls the redox-state and mitochondrial function, whose activity may be modulated by antioxidants. A close link exists between fuel metabolism and mitochondrial biogenesis. The relationship between fuel metabolism and cell survival strongly implies the existence of a shared signaling network, by which hepatocytes respond to challenges of external stimuli. The AMPK pathway may belong to this network. A series of drugs and therapeutic candidates enable hepatocytes to protect mitochondria from radical stress and increase cell viability, which may be associated with the activation of AMPK, liver kinase B1, and other molecules or components. Consequently, the components downstream of AMPK may contribute to stabilizing mitochondrial membrane potential for hepatocyte survival. In this review, we discuss the role of the AMPK pathway in hepatic energy metabolism and hepatocyte viability. This information may help identify ways to prevent and/or treat hepatic diseases caused by the metabolic syndrome. Moreover, clinical drugs and experimental therapeutic candidates that directly or indirectly modulate the AMPK pathway in distinct manners are discussed here with particular emphasis on their effects on fuel metabolism and mitochondrial function. (C) 2010 Baishideng. All rights reserved.
ISSN
1007-9327
Language
English
URI
https://hdl.handle.net/10371/76458
DOI
https://doi.org/10.3748/wjg.v16.i30.3731
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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