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Osteoporos Int. 2018 Aug;29(8):1713-1720. doi: 10.1007/s00198-018-4570-1. Epub 2018 May 18.

Impact of muscle atrophy on bone metabolism and bone strength: implications for muscle-bone crosstalk with aging and disuse.

Author information

1
Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Laney Walker Blvd. CB2915, Augusta, GA, 30912, USA.
2
ASAN Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea.
3
Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Laney Walker Blvd. CB2915, Augusta, GA, 30912, USA. mhamrick@augusta.edu.

Abstract

Bone fractures in older adults are often preceded by a loss of muscle mass and strength. Likewise, bone loss with prolonged bed rest, spinal cord injury, or with exposure to microgravity is also preceded by a rapid loss of muscle mass. Recent studies using animal models in the setting of hindlimb unloading or botulinum toxin (Botox) injection also reveal that muscle loss can induce bone loss. Moreover, muscle-derived factors such as irisin and leptin can inhibit bone loss with unloading, and knockout of catabolic factors in muscle such as the ubiquitin ligase Murf1 or the myokine myostatin can reduce osteoclastogenesis. These findings suggest that therapies targeting muscle in the setting of disuse atrophy may potentially attenuate bone loss, primarily by reducing bone resorption. These potential therapies not only include pharmacological approaches but also interventions such as whole-body vibration coupled with resistance exercise and functional electric stimulation of muscle.

KEYWORDS:

Irisin; Microgravity; Myostatin; Osteoclasts; Resistance training

PMID:
29777277
DOI:
10.1007/s00198-018-4570-1
[Indexed for MEDLINE]

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