Exosomes Derived From Mesenchymal Stem Cells Regulating Myotube Cell Atrophy via NF-κB Signaling Pathway

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

Abstract (original English)

Bone marrow mesenchymal stem cells (BMSCs), with their potential for multidifferentiation and self-replication, are considered effective for repairing damaged tissues. BMSCs can repair and replace damaged tissues by differentiating into effective cells and secreting some cytokines that inhibit inflammation and promote tissue repair. Recent studies suggest that BMSCs' main role in tissue repair may involve the secretion of exosomes (BMSC-Exos). Basic research has shown that exosomes can have significant effects on orthopedic diseases such as osteoarthritis, muscle tissue injury, and fractures by stimulating regeneration and reducing inflammation. However, the effect of exosomes on tumor necrosis factor (TNF-α)-induced muscle atrophy remains unclear. Therefore, this study investigated the mechanism underlying the protective effect of BMSC-Exos on TNF-α-induced C2C12 myotube atrophy. Treatment with TNF-α (20 ng/mL) for 48 h significantly reduced myotube viability and diameter, which were subsequently reversed by treatment with BMSC-Exos. BMSC-Exos treatment suppressed the expression of E3 ubiquitin ligases, including Atrogin‑1/muscle atrophy F‑box and muscle ring‑finger protein‑1 (MuRF-1). Furthermore, it increased the protein expression levels of myoblast determination protein-1 (MyoD) in TNF-α-induced myotubes. BMSC-Exos also decreased the nuclear translocation of nuclear factor

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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