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- W2900538900 endingPage "3558" @default.
- W2900538900 startingPage "3558" @default.
- W2900538900 abstract "Molecular mechanisms that trigger disuse-induced postural muscle atrophy as well as myosin phenotype transformations are poorly studied. This review will summarize the impact of 5' adenosine monophosphate -activated protein kinase (AMPK) activity on mammalian target of rapamycin complex 1 (mTORC1)-signaling, nuclear-cytoplasmic traffic of class IIa histone deacetylases (HDAC), and myosin heavy chain gene expression in mammalian postural muscles (mainly, soleus muscle) under disuse conditions, i.e., withdrawal of weight-bearing from ankle extensors. Based on the current literature and the authors' own experimental data, the present review points out that AMPK plays a key role in the regulation of signaling pathways that determine metabolic, structural, and functional alternations in skeletal muscle fibers under disuse." @default.
- W2900538900 created "2018-11-29" @default.
- W2900538900 creator A5001932478 @default.
- W2900538900 creator A5026803588 @default.
- W2900538900 creator A5077811157 @default.
- W2900538900 date "2018-11-12" @default.
- W2900538900 modified "2023-10-18" @default.
- W2900538900 title "AMP-Activated Protein Kinase as a Key Trigger for the Disuse-Induced Skeletal Muscle Remodeling" @default.
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