Abstract

Mesenchymal stem cells (MSCs) are stem cells with the potential ability to differentiate into various cells and the ability to self-renew and resemble fibroblasts. These cells can adhere to plastic to facilitate the culture process. MSCs can be used in research into tissue biotechnology and rejuvenation medicine. MSCs are also beneficial in recipient tissue and differentiate as a breakthrough strategy through paracrine activity. Many databases have shown MSC-based treatment can be beneficial in the reduction of osteogenesis induced by senescence. In this article, we will discuss the potential effect of MSCs in senescence cells related to osteogenesis.

Highlights

  • extracellular vehicles (EVs) bring enzymes responsible for remodeling processes, such as metalloproteinases and regulators, or directly via secretion of the matrix-remodeling enzyme from the environment of the cells. This process may contribute to tetraspanins and proteoglycans, which alter the interaction between EVs and cells and modify extracellular matrix (ECM)

  • The use of SA-a-Fuc has the potential ability to become a novel senescence marker which increases in response to deoxyribonucleic acid (DNA) damage, replication, and oncogenic activity induced by senescence

  • Deletion of Nicotinamide phosphoribosyl-transferase (Nampt) in mesenchymal lineage cells is associated with a significant decrease in bone density and supports the hypothesis that NAD+ plays a role in osteoblast progenitor but may retard bone formation

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Summary

Introduction

Other known culprits than bone resorption activity are MSC impairment, shifting of osteogenesis to adipogenesis, and decreased capacity for renewal activity [14,15] This imbalance activity may increase the risk of fractures [16]. An increase in reactive oxygen species (ROS) in the mesenchymal lineage, such as stem cells, progenitor of osteoblasts, and osteocytes, contributes to bone formation loss, thereby decreasing osteoblastogenesis [24]. This activity is stimulated by FoxOs activity and binding of the FoxOs to β-catenin. We will discuss the potential effect of MSCs in senescence cells related to osteogenesis

Cell Cycle Arrest
Decreased Telomere Length and Response to DNA Injury
CDKN2A Locus Depression
Stress-Inducing Senescence and ROS
Aging Related Oncogene
The Roles of Extracellular Vesicles
Characteristics of Senescent MSCs
Osteogenesis in Healthy and Senescent MSCs
Conclusions
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