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Activation of serum/glucocorticoid-induced kinase 1 (SGK1) is important to maintain skeletal muscle homeostasis and prevent atrophy.

Authors
  • Andres-Mateos, Eva1
  • Brinkmeier, Heinrich
  • Burks, Tyesha N
  • Mejias, Rebeca
  • Files, Daniel C
  • Steinberger, Martin
  • Soleimani, Arshia
  • Marx, Ruth
  • Simmers, Jessica L
  • Lin, Benjamin
  • Finanger Hedderick, Erika
  • Marr, Tom G
  • Lin, Brian M
  • Hourdé, Christophe
  • Leinwand, Leslie A
  • Kuhl, Dietmar
  • Föller, Michael
  • Vogelsang, Silke
  • Hernandez-Diaz, Ivan
  • Vaughan, Dana K
  • And 3 more
  • 1 McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Type
Published Article
Journal
EMBO Molecular Medicine
Publisher
EMBO
Publication Date
January 2013
Volume
5
Issue
1
Pages
80–91
Identifiers
DOI: 10.1002/emmm.201201443
PMID: 23161797
Source
Medline
License
Unknown

Abstract

Maintaining skeletal muscle mass is essential for general health and prevention of disease progression in various neuromuscular conditions. Currently, no treatments are available to prevent progressive loss of muscle mass in any of these conditions. Hibernating mammals are protected from muscle atrophy despite prolonged periods of immobilization and starvation. Here, we describe a mechanism underlying muscle preservation and translate it to non-hibernating mammals. Although Akt has an established role in skeletal muscle homeostasis, we find that serum- and glucocorticoid-inducible kinase 1 (SGK1) regulates muscle mass maintenance via downregulation of proteolysis and autophagy as well as increased protein synthesis during hibernation. We demonstrate that SGK1 is critical for the maintenance of skeletal muscle homeostasis and function in non-hibernating mammals in normal and atrophic conditions such as starvation and immobilization. Our results identify a novel therapeutic target to combat loss of skeletal muscle mass associated with muscle degeneration and atrophy.

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