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. 2023 Feb 2;14:1087254. doi: 10.3389/fphys.2023.1087254

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Copyright © 2023 Mancinelli and Intini.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Known mechanism of SSPCs aging. In a young organism, the pool of young SSPCs is large, fully functional, and located in a young microenvironment (SSPCs niche) that offers ideal conditions for the SSPCs functions. As the organism becomes older, several mechanisms associated with aging and with a decline of SSPCs regeneration potential are known to happen: 1) the number of the now-aged, but probably still functional, SSPCs reduces (SSPCs exhaustion); 2) some SSPCs become senescent; 3) SSPCs niche conditions change (aged SSPCs niche) due to the chronic inflammation caused by the actively release of SASP factors by both senescent SSPCs within the niche, and neighboring senescent cells (immune, epithelial, endothelial, etc.). In the event of a fracture in elderly individuals the reduced number of SSPCs, the presence of senescent SSPCs, and the chronic inflammation within the aged niche are responsible for the lack of bone formation and fracture healing; a rejuvenation of the niche, by eliminating the inflammation and increasing the number of the functional non-senescent SSPCs, can foster fracture healing. (Created with BioRender.com ).