Satellite cells are clearly necessary for postnatal muscle growth and muscle regeneration in the adult. Satellite cells are normally quiescent and in response to damage become activated, proliferate and differentiate into myocytes that fuse with each other to replace lost myofibers, or fuse with existing myofibers for repair. Following injury, and in neuromuscular degenerative diseases, central nucleation is the hallmark of regenerating myofibers. The role of satellite cells in inflammatory myopathies is less clear, although infiltrating immune cells influence satellite cell activity. The necessity of satellite cells in adult muscle adaptability is equivocal. Although satellite cells are known to participate in adult myofiber hypertrophy, several different mouse models of muscle growth show that they are dispensable; the myonuclear domain is flexible, enlarging to accommodate growth in the absence of satellite cell fusion. Satellite cells are not involved in muscle re-growth following disuse atrophy, as no change in myonuclear number occurs during those processes; myonuclear domain size is reduced with unloading due to decreased cytoplasmic volume and is restored following reloading, independent of satellite cells. Currently, there is also no direct evidence that satellite cells are involved in normal muscle maintenance. Our recent work demonstrates that lifelong satellite cell depletion does not exacerbate sarcopenia; neither the loss of muscle mass nor the attenuated hypertrophic response to overload, both apparent in aged mice, is affected by satellite cells. Thus, whereas satellite cell or stem cell-based therapies for muscle degenerative diseases holds promise, therapies for atrophy focused on increasing satellite cell number or activity are unfounded. The extent to which results from studies of mouse satellite cell properties will be translatable to human muscle remains to be determined.
Disclosure of Interest None Declared