BACKGROUND:Sarcopenia is a chronic condition that leads to strength loss and functional decline,increasing the risk of frailty,disability,falls,and death in older adults.Blood flow restriction training can be effective in the treatment of sarcopenia,but a comprehensive review of its advantages,disadvantages,biological mechanisms,and application options is lacking. OBJECTIVE:To review the advantages,limitations,and biological mechanisms of blood flow restriction training interventions for sarcopenia and to give recommendations for application protocols based on current published evidence. METHODS:A search of major databases was conducted for literature published in the time frame up to February 2023.The search terms were"blood flow restriction training,KAATSU,elderly,sarcopenia,muscle"in English and Chinese.Finally,82 included papers were compiled and analyzed. RESULTS AND CONCLUSION:Blood flow restriction training as an intervention for sarcopenia has been effective in peripheral muscle groups,but there are limitations in its application.Blood flow restriction training is highly operational and safe.This training can improve muscle strength and physical performance,but there are potential risks,including adverse events on skeletal muscle,cardiovascular and endothelial cells.Therefore,blood flow restriction training needs to be performed under scientific guidance and further studies are needed to verify its efficacy in patients with sarcopenia.The biological mechanisms of blood flow restriction training intervention in sarcopenia may include:increasing muscle hypertrophy due to reactive muscle congestion,improving muscle protein synthesis capacity,inducing metabolic stress adaptation,promoting skeletal muscle growth and repair,activating vascular endothelial growth factor signaling pathway to promote angiogenesis,and promoting satellite cell proliferation.However,these specific roles and combined effects of these mechanisms need to be determined by more in-depth studies.Blood flow restriction training interventions for sarcopenia are mainly influenced by training and cuffs.To avoid adverse events,it is recommended that 20%to 50%1RM,20 to 75 repetitions,2 to 3 times per week,30-60 seconds interval between sessions,smaller size cuffs with a pressurization value≤140 mmHg for upper limb training,and larger size cuffs with a pressurization value≤180 mmHg for lower limb training,usually 50%to 80%of the pressure value in the completely occluded artery.However,more research is needed on the training frequency and interval between sessions in older adults,and further research is needed on the optimal choice of cuff pressurization values.

BACKGROUND:Satellite cells are myogenic stem cells located between the muscle fiber membrane and the basement membrane.However,a comprehensive review of the aging mechanisms of satellite cells and their potential mitigation strategies is still lacking.This gap in knowledge hinders the effective guidance for current strategies aimed at attenuating skeletal muscle aging. OBJECTIVE:To review the mechanisms of satellite cell aging in skeletal muscle and the relevant strategies for mitigating this aging process. METHODS:Major databases were searched up to May 2023,including Web of Science,PubMed,China National Knowledge Infrastructure(CNKI),WanFang Data,and VIP.Chinese and English search terms included"skeletal muscle,satellite cells,aging,mechanism,and solution strategy".After strict inclusion and exclusion criteria were applied,78 articles were finally included. RESULTS AND CONCLUSION:(1)Satellite cells,situated between the muscle fiber membrane and basement membrane,possess proliferative and differentiative potential.They usually remain in a quiescent state but become activated in response to muscle tissue stimuli,participating in processes of repair and restoration of normal tissue structure.Aging leads to a reduction in satellite cell numbers,resulting in symptoms such as muscle weakness and decreased endurance.(2)Mechanisms of satellite cell aging primarily involve diminished regenerative capacity,perturbed niche interactions with changing ecology,age-dependent loss,and heterogeneity changes.Reduced satellite cell numbers and activity due to aging lead to slower muscle regeneration and increased injury recovery time.Errors during differentiation may occur,resulting in decreased muscle quality and function deterioration.(3)Strategies for mitigating satellite cell aging encompass modulation of the receptor environment of intra-body satellite cells,peripheral interventions to promote satellite cell regeneration,construction of human muscle models,and exercise and nutritional interventions to induce satellite cell proliferation.These strategies hold promise in offering novel insights and methods for satellite cell regeneration and treatment of skeletal muscle diseases.(4)Future research should delve into the mechanisms of satellite cell aging,explore the interaction between satellite cells and their niches,investigate the relationship of satellite cells with the immune system and mitochondrial function,and develop human muscle models to enhance research depth and accuracy.

Background and Objectives: Human umbilical cord mesenchymal stem cells (HUC-MSCs) are promising candidates for cell-based therapy in regenerative medicine or other diseases due to their superior characteristics, including higher proliferation, faster self-renewal ability, lower immunogenicity, a noninvasive harvest procedure, easy expansion in vitro, and ethical access, compared with stem cells from other sources. Methods: and Results: In the present study, we knocked down the expression of SOX9 in HUC-MSCs by lentivirus interference and found that knockdown of SOX9 inhibited the proliferation and migration of HUC-MSCs and influenced the expression of cytokines (IL-6 and IL-8), growth factors (GM-CSF and VEGF) and stemness-related genes (OCT4 and SALL4). In addition, the repair effect of skin with burn injury in rats treated with HUC-MSCs transfected with sh-control was better than that rats treated with HUC-MSCs transfected with shSOX9 or PBS, and the accessory structures of the skin, including hair follicles and glands, were greater than those in the other groups. We found that knockdown of the expression of SOX9 obviously inhibited the expression of Ki67, CK14 and CK18. Conclusions In conclusion, this study will provide a guide for modifying HUC-MSCs by bioengineering technology in the future.

BACKGROUND:Parkinson's disease is a neurodegenerative disease,and its pathogenesis involves mitochondrial dysfunction.Exercise has a potential ameliorative effect on mitochondrial dysfunction related to Parkinson's disease,but there is no comprehensive review and in-depth analysis in this field. OBJECTIVE:To comprehensively review and analyze mitochondrial dysfunction related to Parkinson's disease and the potential ameliorative effect of exercise,thereby providing new ideas and methods for the treatment and prevention of Parkinson's disease. METHODS:We searched the Web of Science,PubMed,CNKI,WanFang,and VIP databases with the keywords of"mitochondria,mitochondrial function,mitochondrial disease,mitochondrial dysfunction,Parkinson's disease,Parkinson,exercise,physical activity,exercise training,exercise therapy,mitochondrial impairment,mitochondrial damage,mitochondrial defects"in Chinese and"mitochondria,Parkinson's disease,Parkinson disease,physical exercise,exercise,physical activity,mitochondrial dysfunction,mitochondrial damage,mitochondrial impairment,athletic training,exercise training,rehabilitation"in English.A total of 89 articles were included for review and analysis. RESLUTS AND CONCLUSION:Parkinson's disease is closely related to mitochondrial dysfunction,including mitochondrial biogenesis inhibition,reduced autophagy,increased apoptosis,abnormal elevation of Ca2+ concentration,and increased oxidative stress in Parkinson's disease patients.Exercise has a positive effect on mitochondrial dysfunction related to Parkinson's disease,by promoting mitochondrial biogenesisand autophagy,regulating mitochondrial morphology,altering the plasticity of the mitochondrial respiratory chain,and reducing oxidative stress,thus helping to improve the development and progression of Parkinson's disease.However,the detailed mechanism between mitochondrial dysfunction and the ameliorative effect of exercise is still not fully understood,and future clinical studies can be conducted to validate the results of animal models and gain insights into the benefits and mechanisms of exercise in patients with Parkinson's disease.