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

Aging Cell

Christopher L. Mendias³  Konstantin I. Bakhurin¹  Jonathan P. Gumucio²  Mark V. Shallal-Ayzin¹  Carol S. Davis¹ 

[1] Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, USA;Department of Orthopaedic Surgery, University of Michigan Medical School, Ann Arbor, MI, USA;ORCID:orcid.org/0000-0002-2384-0171

关键词: GDF‐8;    longevity;    muscle atrophy;    muscle contractility;    myostatin;    sarcopenia;    skeletal muscle;   

DOI  :  10.1111/acel.12339

来源: Wiley

【 摘 要 】

Summary

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.

【 授权许可】

CC BY   
© 2015 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

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