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Int J Biochem Cell Biol. 2013 Oct;45(10):2200-8. doi: 10.1016/j.biocel.2013.06.011. Epub 2013 Jun 22.

Disuse-induced muscle wasting.

Author information

1
Department of Neurobiology, Physiology and Behavior, University of California, Davis, One Shields Avenue, Davis, CA 95616, United States. scbodine@ucdavis.edu

Abstract

Loss of skeletal muscle mass occurs frequently in clinical settings in response to joint immobilization and bed rest, and is induced by a combination of unloading and inactivity. Disuse-induced atrophy will likely affect every person in his or her lifetime, and can be debilitating especially in the elderly. Currently there are no good therapies to treat disuse-induced muscle atrophy, in part, due to a lack of understanding of the cellular and molecular mechanisms responsible for the induction and maintenance of muscle atrophy. Our current understanding of disuse atrophy comes from the investigation of a variety of models (joint immobilization, hindlimb unloading, bed rest, spinal cord injury) in both animals and humans. Under conditions of unloading, it is widely accepted that there is a decrease in protein synthesis, however, the role of protein degradation, especially in humans, is debated. This review will examine the current understanding of the molecular and cellular mechanisms regulating muscle loss under disuse conditions, discussing the similarities and areas of dispute between the animal and human literature. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.

KEYWORDS:

Protein degradation; Protein synthesis; Reloading; Ubiquitin ligases; Unloading

PMID:
23800384
PMCID:
PMC3856924
DOI:
10.1016/j.biocel.2013.06.011
[Indexed for MEDLINE]
Free PMC Article

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