Journal
BONE
Volume 146, Issue -, Pages -Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2021.115886
Keywords
Magnesium; Aging; Muscle stem cell; Myogenic differentiation; Muscle regeneration; Sarcopenia
Categories
Funding
- Science and Technology Innovation Commission of Shenzhen Municipality, China [JCYJ2018030 5164659637, JCYJ20190806160407178, JSGG20180504170427135, SGLH20180625141602256, JCYJ20180305164544288, JCYJ201704 1362104773]
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The study found that promoting myogenic differentiation and myotube hypertrophy in aged muscle can be achieved through an appropriate environment of magnesium (Mg2+), which activates the mTOR signaling pathway. This provides a promising therapeutic strategy for treating MuSC dysfunction and sarcopenia in the elderly through Mg2+ supplementation.
Magnesium (Mg2+), as an essential mineral, supports and sustains the health and activity of the organs of the human body. Despite some clinical evidence on the association of Mg2+ deficiency with muscle regeneration dysfunction and sarcopenia in older-aged individuals, there is no consensus on the action mode and molecular mechanism by which Mg2+ influences aged muscle size and function. Here, we identified the appropriate Mg2+ environment that promotes the myogenic differentiation and myotube hypertrophy in both C2C12 myoblast and primary aged muscle stem cell (MuSC). Through animal experiments, we demonstrated that Mg2+ supplementation in aged mice significantly promotes muscle regeneration and conserves muscle mass and strength. Mechanistically, Mg2+ stimulation activated the mammalian target of rapamycin (mTOR) signalling, inducing the myogenic differentiation and protein synthesis, which consequently offers protections against the age-related decline in muscle regenerative potential and muscle mass. These findings collectively provide a promising therapeutic strategy for MuSC dysfunction and sarcopenia through Mg2+ supplementation in the elderly.
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