Skeletal muscle phenotype plays a critical role in human performance and health, and skeletal muscle oxidative capacity is a key determinant of exercise tolerance. More recently, defective muscle oxidative metabolism has been implicated in a number of conditions associated with the metabolic syndrome, cardiovascular disease and muscle-wasting disorders. AMPK (AMP-activated protein kinase) is a critical regulator of cellular and organismal energy balance. AMPK has also emerged as a key regulator of skeletal muscle oxidative function, including metabolic enzyme expression, mitochondrial biogenesis and angiogenesis. AMPK mediates these processes primarily through alterations in gene expression. The present review examines the role of AMPK in skeletal muscle transcription and provides an overview of the known transcriptional substrates mediating the effects of AMPK on skeletal muscle phenotype.
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April 2010
Review Article|
January 26 2010
AMPK-mediated regulation of transcription in skeletal muscle
Sean L. McGee
;
*School of Medicine, Deakin University, Geelong, Victoria 3217, Australia
Correspondence: Dr Sean L. McGee (sean.mcgee@deakin.edu.au).
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Mark Hargreaves
Mark Hargreaves
†Department of Physiology, The University of Melbourne, Parkville, Victoria 3010, Australia
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Clin Sci (Lond) (2010) 118 (8): 507–518.
Article history
Received:
October 21 2009
Revision Received:
December 03 2009
Accepted:
December 14 2009
Citation
Sean L. McGee, Mark Hargreaves; AMPK-mediated regulation of transcription in skeletal muscle. Clin Sci (Lond) 1 April 2010; 118 (8): 507–518. doi: https://doi.org/10.1042/CS20090533
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