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Human muscle stem cells are refractory to aging
Author(s) -
Novak James S.,
Mázala Davi A. G.,
Nearing Marie,
Hindupur Ravi,
Uapinyoying Prech,
Habib Nayab F.,
Dickson Tessa,
Ioffe Olga B.,
Harris Brent T.,
FideliaLambert Marie N.,
Rossi Christopher T.,
Hill D. Ashely,
Wagner Kathryn R.,
Hoffman Eric P.,
Partridge Terence A.
Publication year - 2021
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.13411
Subject(s) - biology , regeneration (biology) , limiting , myocyte , stem cell , muscle mass , skeletal muscle , microbiology and biotechnology , function (biology) , anatomy , endocrinology , mechanical engineering , engineering
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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