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BACKGROUND: Mesenchymal stem cells are multipotent stromal cells isolated from bone marrow, fat, umbilical cord and other tissues. It can differentiate into different cell types and secrete a variety of proteins with therapeutic potential, which has a good application prospect in the repair of muscle tissue. OBJECTIVE: To review the research progress of mesenchymal stem cells in promoting muscle tissue repair and provide a theoretical basis for further clinical application. METHODS: Relevant articles published from inception to 2022 were retrieved from CNKI, VIP, WanFang, PubMed, Embase and Web of Science databases. The keywords were “mesenchymal stem cells, muscle tissue, muscle injury, muscle atrophy, exosomes, scaffolds” in Chinese and English. The literature about mesenchymal stem cell migration promoting muscle fiber proliferation and repair was screened. Finally, 98 articles were included for review and analysis. RESULTS AND CONCLUSION: (1) The related mechanisms of mesenchymal stem cell migration promoting muscle fiber proliferation and repair are complex, mostly by anti-inflammatory, inhibiting interstitial fibrosis, inhibiting the fat formation and other ways to promote muscle fiber proliferation and repair. (2) The related biological scaffolds and cell co-culture based on mesenchymal stem cells can significantly compensate for the low survival rate of mesenchymal stem cells after colonization. (3) At present, mesenchymal stem cell therapy still has apparent limitations. In the future, mesenchymal stem cells combined with other therapies should become the primary development trend. [ABSTRACT FROM AUTHOR]

BACKGROUND: Skeletal muscle is the main tissue to maintain human health, and sarcopenia affects people’s health and quality of life. Muscle satellite cells are skeletal muscle stem cells activated to proliferate and differentiate when stimulated by exercise, promote muscle hypertrophy, and delay the occurrence of sarcopenia. OBJECTIVE: To provide exercise prevention and treatment guidance for age-related sarcopenia, muscle atrophy, and muscle injury repair, and provide theoretical support for subsequent research. METHODS: CNKI, PubMed, and Web of Science were searched for relevant documents published from 2010 to 2020 with the keywords of “skeletal muscle, satellite cells, proliferation, differentiation, muscle repair, scrcopenia” in Chinese and English, respectively. After initial screening of titles and abstracts, 100 articles were included for review. RESULTS AND CONCLUSION: There are many studies on the proliferation and differentiation of exercise-activated muscle satellite cells. Compared with endurance exercise (aerobic), resistance exercise has a significant effect. Different types of exercises can activate the proliferation and differentiation of different types of muscle satellite cells. Factors such as exercise intensity, load threshold, exercise time and frequency all influence the degree of satellite cell activation, proliferation and differentiation. Research on the interaction between exercise-activated muscle satellite cell proliferation and differentiation signaling pathways is insufficient, and it is found that exercise can regulate muscle extracellular matrix, oxidative stress levels, and autophagy to improve sarcopenia. How exercise activates the signal pathways of muscle satellite cell proliferation and differentiation to effectively promote synergy requires more in-depth research and exploration. [ABSTRACT FROM AUTHOR]

Objective To investigate the relationship between beta enolase gene two point rs121918403 (G/A), rs121918404 (G/A) polymorphism with skeletal muscle Atrophy in the patient with chronic obstructive pulmonary disease (COPD). Method Beta enolase genes were assayed by polymerase chain and one-way directed sequencing methods between 120 COPD patients and 60 age-matched controls in Kunming. Result There was no mutation in rs121918403 (G/A) and rs121918404 (G/A) of beta enolase gene in COPD patients and healthy subjects. Conclusion SNPs of two mutational sites of beta enolase are not correlated to skeletal muscle atrophy in COPD patients in Kunming. [ABSTRACT FROM AUTHOR]