Abstract
Skeletal muscle is a striated tissue composed of multinucleated fibers that contract under the control of the somatic nervous system to direct movement. The stem cells of skeletal muscle, known as satellite cells, are responsible for muscle fiber growth, turnover, and regeneration. Satellite cells are activated and proliferate in response to stimuli, and simplistically, have two main fates—to repopulate the satellite cell niche, or differentiate to regenerate or repair muscle fibers. However, the ability to regenerate muscle and replace lost myofibers declines with age. This loss of function may be a result of extrinsic changes in the niche, such as alterations in signaling or modifications to the extracellular matrix. However, intrinsic epigenetic changes within satellite cells may also affect cell fate and cause a decline in regenerative capacity. This review will describe the mechanisms that regulate cell fate decisions in adult skeletal muscle, and how changes during aging affect muscle fiber turnover and regeneration.
Highlights
Skeletal muscle is a striated tissue composed of multinucleated fibers that contract under the control of the somatic nervous system to direct movement
Stem cells are thought to be protected from the effects of aging by quiescence, a state of cellular hibernation which provides cushioning from the stresses associated with cell proliferation, thereby limiting cellular damage
Aging is associated with the inability to maintain stem cell quiescence, which increases the chances of stem cell damage, and results in a loss of stem cell selfrenewal and regenerative capacity
Summary
Skeletal muscle is a striated tissue composed of multinucleated fibers that contract under the control of the somatic nervous system to direct movement. It is possible that the small number of satellite cells that remain in tamoxifen-treated mice provides enough cells to maintain muscle mass until other age-related changes occur, at which point loss of satellite cell function manifests as sarcopenia. Persistent TGFβ and Wnt signaling during aging leads to accumulation of skeletal muscle fibrosis, which disrupts basal lamina architecture, and reduces satellite cell proliferation and self-renewal.
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