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Aging Cell. 2015 Aug;14(4):704-6. doi: 10.1111/acel.12339. Epub 2015 Mar 24.

Haploinsufficiency of myostatin protects against aging-related declines in muscle function and enhances the longevity of mice.

Author information

1
Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA.
2
Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, USA.

Abstract

The molecular mechanisms behind aging-related declines in muscle function are not well understood, but the growth factor myostatin (MSTN) appears to play an important role in this process. Additionally, epidemiological studies have identified a positive correlation between skeletal muscle mass and longevity. Given the role of myostatin in regulating muscle size, and the correlation between muscle mass and longevity, we tested the hypotheses that the deficiency of myostatin would protect oldest-old mice (28-30 months old) from an aging-related loss in muscle size and contractility, and would extend the maximum lifespan of mice. We found that MSTN(+/-) and MSTN(-/-) mice were protected from aging-related declines in muscle mass and contractility. While no differences were detected between MSTN(+/+) and MSTN(-/-) mice, MSTN(+/-) mice had an approximately 15% increase in maximal lifespan. These results suggest that targeting myostatin may protect against aging-related changes in skeletal muscle and contribute to enhanced longevity.

KEYWORDS:

GDF-8; longevity; muscle atrophy; muscle contractility; myostatin; sarcopenia; skeletal muscle

PMID:
25808276
PMCID:
PMC4531085
DOI:
10.1111/acel.12339
[Indexed for MEDLINE]
Free PMC Article

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