Evidence map›Paper›PMID 39901193›Full record

ArticleStem cell research & therapy2025

hBMSC-EVs alleviate weightlessness-induced skeletal muscle atrophy by suppressing oxidative stress and inflammation.

Mengyuan Chang, Ruiqi Liu, Bingqian Chen, Jin Xu, Wei Wang, Yanan Ji, Zihui Gao, Boya Liu, Xinlei Yao, Hualin Sun and 2 more

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Mengyuan Chang *Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.
Ruiqi Liu *Department of Clinical Medicine, Medical College, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.
Bingqian Chen *Department of Orthopedics, First People's Hospital of Changshu City, Changshu Hospital Affiliated to Soochow University, Changshu, 215500, Jiangsu Province, People's Republic of China.
Jin XuDepartment of Basic Medicine, Kangda College of Nanjing Medical University, Lianyungang, 222000, Jiangsu Province, People's Republic of China.
Wei WangKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.
Yanan JiKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.
Zihui GaoKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.
Boya LiuKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.
Xinlei YaoKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.
Hualin SunKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China. sunhl@ntu.edu.cn.
Feng XuDepartment of Endocrinology, Affiliated Hospital 2 of Nantong University and First People's Hospital of Nantong City, Nantong, 226001, Jiangsu Province, People's Republic of China. xufeng5205529@163.com.
Yuntian ShenKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China. syt517@ntu.edu.cn.ORCID http://orcid.org/0000-0002-5145-4761

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMuscle disuse and offloading in microgravity are likely the primary factors mediating spaceflight-induced muscle atrophy, for which there is currently no effective treatment other than exercise. Extracellular vesicles derived from bone marrow mesenchymal stem cells (BMSC-EVs) possess anti-inflammatory and antioxidant properties, offering a potential strategy for combating weightless muscular atrophy.

methodsIn this study, human BMSCs-EVs (hBMSC-EVs) were isolated using super-centrifugation and characterized. C2C12 myotube nutrition-deprivation and mice tail suspension models were established. Subsequently, the diameter of C2C12 myotubes, Soleus mass, cross-sectional area (CSA) of muscle fibers, and grip strength in mice were assessed to investigate the impact of hBMSC-EVs on muscle atrophy. Immunostaining, transmission electron microscopy observation, and western blot analysis were employed to assess the impact of hBMSC-EVs on muscle fiber types, ROS levels, inflammation, ubiquitin-proteasome system activity, and autophagy lysosome pathway activation in skeletal muscle atrophy.

resultsThe active hBMSC-EVs can be internalized by C2C12 myotubes and skeletal muscle. hBMSC-EVs can effectively reduce C2C12 myotube atrophy caused by nutritional deprivation, with a concentration of 10 × 10

conclusionsOur findings indicate that hBMSC-EVs are capable of inhibiting excessive activation of the UPS and autophagy lysosome pathway, suppressing oxidative stress and inflammatory response, reversing muscle fiber type transformation, effectively delaying hindlimb unloading-induced muscle atrophy and enhancing muscle function. Our study has further advanced the understanding of the molecular mechanism underlying muscle atrophy in weightlessness and has demonstrated the protective effect of hBMSC-EVs on muscle atrophy.

Indexed as

InflammationMesenchymal Stem CellsMuscular AtrophyOxidative StressWeightlessnessAnimalsAutophagyCell LineHindlimb SuspensionHumansMaleMiceMice, Inbred C57BLMuscle Fibers, SkeletalMuscle, SkeletalBone marrow mesenchymal stem cellsExtracellular vesiclesInflammationMuscle atrophyOxidative stress

Identifiers

PMID39901193
PMCPMC11792267

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.