Published online Sep 26, 2019. doi: 10.4252/wjsc.v11.i9.677
Peer-review started: March 4, 2019
First decision: August 1, 2019
Revised: August 15, 2019
Accepted: September 4, 2019
Article in press: September 4, 2019
Published online: September 26, 2019
Processing time: 209 Days and 14.7 Hours
Tendon ageing is a complicated process caused by multifaceted pathways and ageing plays a critical role in the occurrence and severity of tendon injury. The role of tendon stem/progenitor cells (TSPCs) in tendon maintenance and regeneration has received increasing attention in recent years. The decreased capacity of TSPCs in seniors contributes to impaired tendon functions and raises questions as to what extent these cells either affect, or cause ageing, and whether these age-related cellular alterations are caused by intrinsic factors or the cellular environment. In this review, recent discoveries concerning the biological characteristics of TSPCs and age-related changes in TSPCs, including the effects of cellular epigenetic alterations and the mechanisms involved in the ageing process, are analyzed. During the ageing process, TSPCs ageing might occur as a natural part of the tendon ageing, but could also result from decreased levels of growth factor, hormone deficits and changes in other related factors. Here, we discuss methods that might induce the rejuvenation of TSPC functions that are impaired during ageing, including moderate exercise, cell extracellular matrix condition, growth factors and hormones; these methods aim to rejuvenate the features of youthfulness with the ultimate goal of improving human health during ageing.
Core tip: Tendon stem/progenitor cells (TSPCs) play an essential role in tendon maintenance, regeneration and repair. Recent studies indicate that an association between the decreased capacities of aged TSPCs and the impaired tendon functions observed with increasing age. In this review, we briefly discuss novel updates in research investigating TSPCs characteristics. Then, we summarize the epigenetic variations in TSPCs that occur with ageing and provide a detailed description of the pathways that play essential roles in the cellular ageing process. Finally, we propose potential methods to rejuvenate ageing TSPCs and provide additional therapeutic targets for the treatment of age-related tendon diseases.