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The stem cells responsible for maintaining muscle tissue decline in function with age, becoming ever less active. This loss of function contributes to sarcopenia, the characteristic decline in muscle mass and strength that takes place with advancing age. Researchers here report on investigations of the role of adipogenic progenitor cells in the decline of muscle stem cell function. These progenitor cells are a necessary part of the muscle stem cell niche, but their behavior changes for the worse with advancing age, disrupting the balance of intracellular signaling needed for stem cell function.
Declining stem cell function during aging leads to impaired tissue function and contributes to delayed tissue repair following damage. In adult skeletal muscle, loss of myofiber integrity caused by mechanical injuries or diseases are repaired by resident muscle stem cells (MuSCs), called satellite cells, which promptly exit from quiescence after disruption of muscle architecture to expand, differentiate, and drive tissue regeneration. The fate of MuSCs fundamentally depends on the “niche”, their local environment, which is orchestrated by diverse cellular and acellular elements.
Fibro/adipogenic progenitors (FAPs) constitute a population of interstitial mesenchymal cells in skeletal muscle which are devoid of myogenic potential, but support muscle stem cell commitment and can differentiate to the adipogenic or fibrotic lineages. A recent study demonstrated an important function of FAPs in maintaining long-term homeostasis of skeletal muscle: long term in-vivo depletion of FAPs decreased the number of MuSCs and reduced muscle mass and strength, suggesting a critical role of FAPs in maintaining the stem cell pool and sustaining myofiber growth and turnover.
The decline of MuSC function and muscle regenerative capacity during aging is under the control of a wide range of signals, out of which many arise from extrinsic cues coming from the local or systemic environment. A recent study investigated how aging influences the fate of FAPs and their cross-talk with MuSCs to regulate the balance between myogenesis, adipogenesis and fibrosis in skeletal muscle. Aging causes a clonal selection of FAPs, which favors their fibrogenic over adipogenic conversion. Interestingly, aged FAPs fail to efficiently amplify following muscle injury and aging alters the capacity of FAPs to support MuSC amplification and commitment. Both in-vitro co-culture and in-vivo transplantation of young FAPs rejuvenate aged MuSC function, but aged FAPs lose the ability to efficiently support MuSCs. The fact that the support of FAPs to MuSCs is communicable via conditioned medium suggested that soluble factors regulate this paracrine cross-talk.
Future research will be necessary to further dissect FAP function during homeostasis and tissue repair and unravel how the heterogeneity of this population is orchestrated in health and disease. In particular, the signals that mediate FAP dysfunction and the spatio-temporal control of their fate and interactions with MuSCs will be key to understand how aging of different compartments of the stem cell niche contribute to global regenerative capacity.
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