Aging of the Organs and Systems: 3 (Biology of Aging and its Modulation)


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By comparing genome-wide RNA microarray data obtained from human Y-TSPCs and A-TSPCs, an intriguing difference was found: Altered genes were mainly distributed in categories such as cell—cell contact, cell adhesion, motility, migration, cytoskeleton and actin-associated transcripts, which might be the cause of the phenotypic and behavioral variations in A-TSPCs.

In addition, the changes in features related to actin in A-TSPCs also significantly disrupted the formation of actin stress fibers and cell-matrix interactions[ 14 ]. P16 overexpression was responsible for the decrease in the tenogenic differentiation capacity of young TSPCs, and an analysis of the underlying mechanism revealed that this effect was mediated by P16, which enhanced the expression of miR and subsequently inhibited the production of its direct target EGR1.

Thus, a decrease in EphA4 and EphB2 production with ageing contributes to the limited cell—cell interactions and decreased cell proliferation, motility and actin turnover that play essential roles in the human TSPC ageing process, changes that are potentially mediated by the abovementioned pathways[ 56 ].

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As a result of in-depth explorations of age-related changes in TSPCs during the cellular ageing process, scholars are now more likely to develop methods to reverse the deficits in TSPC function that result from advanced age. Numerous factors, including macroscopic factors associated with an the uncomfortable exercise intensity and microscopic factors associated with an impaired estrogen balance, deteriorated ECM conditions and inappropriate drug use, alter the features of TSPCs, particularly during ageing, and these alterations are mainly deleterious to TSPC function and the maintenance of tendon homeostasis.

Furthermore, repair might be achieved by adjusting these factors, which have potential roles in the rejuvenation of aged TSPCs and are listed in Figure 1. MTR has also been studied to determine the effects of motion on wound healing in aged tendons[ 75 ], resulting in faster healing and a better healing quality through the restoration of the TSPC pool, which is beneficial for delaying TSPC senescence, enhancing the production of collagen fibers and reversing the erroneous differentiation of TSPCs.

This approach eventually reverses the histopathological alterations that observed in subjects with age-related tendon diseases[ 76 - 78 ]. Furthermore, the role of moderate exercise in the effects of ageing on TSPCs has been investigated. Moderate exercise ameliorates the depletion of the TSPC pool by up-regulating the expression of cell proliferation and stem cell markers coupled with decreased lipid deposition, proteoglycan accumulation and calcification formation, and it is beneficial for delaying the undesirable effects of age[ 15 ].

Pin 1 plays an important role in delaying the TSPC senescence process, which was confirmed by the decreased production of senescence markers and P16 and increased telomerase activity coupled with the opposite results following transfection with the Pin1-siRNA.

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Overexpression of Pin1 also effectively deferred late-stage TSPC senescence progression, but had no evident effect on the progression of early-stage cellular senescence, and miRp was involved in regulating of Pin1 production, leading to a substantial decrease in Pin1 expression. Notably, miRa also has a crucial role in modulating TSPCs senescence by facilitating the proliferation, migration and tenogenic differentiation of these cells and decreasing the expression of senescence markers inhibiting target downstream molecules of ROCK1 activity[ 63 ], revealing that the blockade of ROCK activity is another promising strategy for combating TSPC ageing.

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Culture-expanded TSPCs an in vitro ageing process tend to exhibit a loss of phenotype, resulting in impaired function of TSPC, and Zhang et al[ 65 ] found that altered gene expression was related to the increased activity and expression of Hdac subtypes with passaging. Overall, these molecules and their functional states represent potential therapeutic targets for reversing age-related pathological changes in TSPCs. Moreover, the activation of EphA4 or EphB2-dependent pathways reverses these harmful consequences, further revealing essential roles in preventing TSPC ageing.

At the same time, IGF-1 promotes the proliferation and maintenance of TSPC phenotypes by increasing the expression of decorin and scleraxis[ 40 ], indicating that the altered fate of TSPCs is able to be reversed by modulating the relative expression levels of hormones. In addition, rapamycin slows ageing in mice[ 82 , 83 ], and metformin, pentosidine and multiflorum increase the lifespans of animals and humans[ 84 - 86 ]. However, the relationships between these drugs and the mechanisms underlying the increase in lifespans are unknown due to the limited and insufficient number of studies conducted in this area[ 84 - 86 ].

Additionally, based on most recent development in regenerative medicine, Dale et al[ 87 ] induced human embryonic stem cells to differentiate into tendon-like cells in the presence of exogenous bone morphogenetic protein BMP 12 and BMP 13 and directed parthenogenetic stem cells to differentiate into tenocytes. Moreover, mechanical stretching improved the tenogenic differentiation of pMSCs[ 88 ]. Similar results were also obtained using iPSCs[ 89 , 90 ]. Thus, these cells may represent an exogenous supplementation to TSPCs or tenocytes, which is also an ideal way to method for rejuvenating ageing of tendons and provides alternative healing strategies for reversing tendon ageing in the future.

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TSPCs sustain regeneration at the site of tendon injury, and the loss of their function with advanced age causes aged-related tendon diseases. Although limited studies have been performed and the conclusions regarding the altered differentiation capacities and mechanisms involved are controversial, particularly regarding the erroneous differentiation, researchers generally agree that the cell number and tenogenic differentiation decrease with ageing, providing future directions for studies of TSPCs ageing. In particular, alterations in the ECM environment have been shown to re-establish the regenerative capacity of aged TSPCs, indicating that alterations in stem cell activity may be tractable for intervention, a hypothesis that is supported by the effects of alterations in cell-intrinsic pathways involved in TSPC ageing.

Because humans are living longer, improvements in our understanding of the mechanistic networks underlying the age-associated in TSPCs and the tendon repair ability are critical for combating age-related tendon diseases. Advanced Search.


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All rights reserved. World J Stem Cells. Author contributions : Dai GC conceived the idea for the paper and completed the majority of the writing; Li YJ provided assistance with writing and performed a search for relevant publications; Chen MH prepared the figure and table; Lu PP provided input during the drafting of the paper; Rui YF revised and proofread the paper. Conflict-of-interest statement : All authors declare that they have no conflicts of interest, financial or otherwise to report. Open-Access : This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers.

Factor Cell source Interventional details Results Ref. Ageing and cell differentiation. Ageing and cell specific cluster differentiation CD markers. Ageing and cell stemness markers. Ageing and cell viscoelasticity. Ageing and cell senescence markers. Mechanisms involved in the ageing process. MiRp reduces the expression of pin1 that downregulates the expression of P16 and ultimately delays TSPCs ageing.

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PmiREGR1 pathway negatively modulates the cell tenogenic differentiation and senescence process. Additionally, there are many cell external environment conditions, such as moderate treadmill running, moderate exercise, young decellularized extracellular matrix and young hypoxic-conditioned culture medium, can rejuvenate age-related alterations in aged-TSPCs. Curr Stem Cell Res Ther. Agabalyan N. Tendinopathy — from basic science to treatment. Int J Exp Pathol. The impact of aging on rotator cuff tear size. Musculoskelet Surg. Age-related changes in the biomechanics of healing patellar tendon.

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Aging of the Organs and Systems: 3 (Biology of Aging and its Modulation) Aging of the Organs and Systems: 3 (Biology of Aging and its Modulation)
Aging of the Organs and Systems: 3 (Biology of Aging and its Modulation) Aging of the Organs and Systems: 3 (Biology of Aging and its Modulation)
Aging of the Organs and Systems: 3 (Biology of Aging and its Modulation) Aging of the Organs and Systems: 3 (Biology of Aging and its Modulation)
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Aging of the Organs and Systems: 3 (Biology of Aging and its Modulation) Aging of the Organs and Systems: 3 (Biology of Aging and its Modulation)
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