C2C12-Derived ApoVs Promote Skeletal Muscle Development and Ameliorate Age-Related Muscle Loss Through Igf1r/PI3K/AKT/mTOR Pathway
Jiang A., Liu Y., Wang L., Wang H., Wu S., Bao W.
Animal Study, published in J Cachexia Sarcopenia Muscle (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- J Cachexia Sarcopenia Muscle (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41344911
- PMCID
- PMC12678004
- DOI
- 10.1002/jcsm.70159
- Citations
- 1
Abstract (original English)
Background Apoptosis coincides with the differentiation of skeletal myoblasts, and numerous studies have shown that the apoptotic activity is required for myogenic differentiation. Although the role of apoptosis in skeletal muscle differentiation has been well documented, its mechanism is largely unknown. Methods Apoptotic extracellular vesicles (apoVs) were extracted from differentiated C2C12 cells or STS-treated undifferentiated C2C12 myoblasts. C2C12 myoblasts, 8-week-old male mice or 15-month-old male mice were used as in vitro and in vivo models, respectively. These models were treated with C2C12-derived apoVs to explore the biological function and mechanism of apoVs in myogenic differentiation, skeletal muscle development and aging. Results Proteomic analysis revealed that inhibition of apoptotic activity by Z-VAD-FMK (ZVAD) affected extracellular components. Using immunofluorescence staining, western blotting and transmission electron microscopy analysis, our results demonstrated the generation of apoVs during myogenic differentiation. C2C12-derived apoVs exhibited a typical double-membrane spherical structure, phosphatidylserine exposure and were highly positive for the general apoV markers cleaved caspase 3 (CASP3), Alix and TSG101. Inhibition of apoptotic activity significantly reduced (p = 0.0029) the protein level of myosin heavy chain (1.05 in the Con group vs. 0.3
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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