ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
Danshensu sodium salt alleviates muscle atrophy via CaMKII-PGC1α-FoxO3a signaling pathway in D-galactose-induced models.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Article
- Macrophage-Myocyte Cross Talk Induces M1 Polarization and Inflammatory Cytokine Production During Cancer Cachexia.Mediators of inflammation · 2026Article
- Mitochondrial ROS dyshomeostasis: a key driver of accelerated supraspinatus atrophy after rotator cuff injury.Frontiers in physiology · 2026Review
- Effects of alpha-ketoisocaproate in oxidative stress-induced C2C12 myotubes via inhibition of p38 MAPK and ERK1/2.Biochemistry and biophysics reports · 2025Article
- Danshensu sodium salt alleviates muscle atrophy via CaMKII-PGC1α-FoxO3a signaling pathway in D-galactose-induced models.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
Sarcopenia is an age-related muscle atrophy syndrome characterized by the loss of muscle strength and mass. Although many agents have been used to treat sarcopenia, there are no successful treatments to date. In this study, we identified Danshensu sodium salt (DSS) as a substantial suppressive agent of muscle atrophy. We used a D-galactose (DG)-induced aging-acceleration model, both in vivo and in vitro, to confirm the effect of DSS on sarcopenia. DSS inhibits the expression of muscle atrophy-related factors (MuRF1, MAFbx, myostatin, and FoxO3a) in DG-induced mouse C2C12 and human skeletal muscle cells. Additionally, DSS restored the diameter of reduced C2C12 myotubes. Next, we demonstrated that DSS stimulates AMPK and PGC1α through CaMKII. DSS inhibits the translocation of FoxO3a into the nucleus, thus inhibiting muscle atrophy in a calcium-dependent manner. DSS initiated the protein-protein interaction between FoxO3a and PGC1α. The reduction of the PGC1α-FoxO3a interaction by DG was restored by DSS. Also, DSS suppressed increased intracellular reactive oxygen species (ROS) by DG. In animal models, DSS administration improved mouse muscle mass and physical performance (grip strength and hanging test) under DG-induced accelerated aging conditions. These findings demonstrated that DSS attenuates muscle atrophy by inhibiting the expression of muscle atrophy-related factors. Therefore, DSS may be a potential therapeutic agent for the treatment of sarcopenia.
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