4.7 Article

Human muscle stem cells are refractory to aging

期刊

AGING CELL
卷 20, 期 7, 页码 -

出版社

WILEY
DOI: 10.1111/acel.13411

关键词

aging; human satellite cells; muscle regeneration; myogenic capacity; sarcopenia

资金

  1. Muscular Dystrophy Association [MDA295203, MDA480160]
  2. Duchenne Parent Project
  3. National Institute of Arthritis and Musculoskeletal and Skin Diseases [R21AG051260, T32AR056993]
  4. Foundation to Eradicate Duchenne
  5. Parent Project Muscular Dystrophy

向作者/读者索取更多资源

The age-related loss of muscle mass and strength is likely not caused by intrinsic loss of myogenicity in satellite cells, but rather by progressive and detrimental changes in the muscle microenvironment that affect the myogenic function of these cells.
Age-related loss of muscle mass and strength is widely attributed to limitation in the capacity of muscle resident satellite cells to perform their myogenic function. This idea contains two notions that have not been comprehensively evaluated by experiment. First, it entails the idea that we damage and lose substantial amounts of muscle in the course of our normal daily activities. Second, it suggests that mechanisms of muscle repair are in some way exhausted, thus limiting muscle regeneration. A third potential option is that the aged environment becomes inimical to the conduct of muscle regeneration. In the present study, we used our established model of human muscle xenografting to test whether muscle samples taken from cadavers, of a range of ages, maintained their myogenic potential after being transplanted into immunodeficient mice. We find no measurable difference in regeneration across the range of ages investigated up to 78 years of age. Moreover, we report that satellite cells maintained their myogenic capacity even when muscles were grafted 11 days postmortem in our model. We conclude that the loss of muscle mass with increasing age is not attributable to any intrinsic loss of myogenicity and is most likely a reflection of progressive and detrimental changes in the muscle microenvironment such as to disfavor the myogenic function of these cells.

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