ArticleJournal of cachexia, sarcopenia and muscle2025
ARC-18 Improved Motor Performance Through Inhibiting ACLY-Mediated Smad2/3 Acetylation in a Model of Duchenne Muscular Dystrophy.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- MD2-IN-1 restores microglial lysosomal function and attenuates amyloid pathology through TREM2-associated signaling in 5×FAD mice.Acta pharmacologica Sinica · 2026Article
- ACLY alleviates cerebral ischemia/reperfusion injury by reducing oxidative stress and enhancing mitochondrial function via histone acetylation.Cell death & disease · 2026Article
- ARC-18 Improved Motor Performance Through Inhibiting ACLY-Mediated Smad2/3 Acetylation in a Model of Duchenne Muscular Dystrophy.Journal of cachexia, sarcopenia and muscle · 2025Article
- Association between geriatric nutritional risk index and fecal incontinence in individuals with stroke: mediating roles of systemic immune inflammation index and oxidative balance scores.Frontiers in nutrition · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundDuchenne muscular dystrophy (DMD) is a genetic disorder characterized by progressive muscle weakness, with inflammation and fibrosis contributing to its pathogenesis. Despite advancements in genetic disease-modifying treatment, there is currently no effective pharmacological treatment for DMD.
methodsNew compound ARC-18, a derivative of Arctigenin known for its anti-inflammatory activity, was designed and synthesized in our lab and administered prophylactically to 2-month-old mdx mice for 60 days. The motor performance was investigated by rotarod test, climbing-pole test, grip strength test, hanging endurance test, treadmill endurance test and gait analysis. Afterwards, molecular biological experiments, including proteomics, immunohistochemistry, immunofluorescence, western blots, gene transfection and immunoprecipitation, were employed to investigate the molecular mechanism of ARC-18 in the treatment of mdx.
resultsARC-18 significantly ameliorated the motor performance of DMD mice (rotating time +65.9%, p < 0.01; hanging time +59.7%, p < 0.05; grip strength +32.1%, p < 0.0001; climbing time -29.0%, p < 0.0001; numbers of electric shocks -69.3%, p < 0.01) by up-regulating the expression of dystrophin-associated proteins (dystrophin, p < 0.01; α-dystroglycan, p < 0.01) and down-regulating the expression of muscle satellite/stem cell proteins (Pax7, p < 0.05; Myod, p < 0.05; Myog, p < 0.05; α-SMA, p < 0.01; fibronectin, p < 0.001; collagen I, p < 0.05). ARC-18 prevented the progression of muscle fibrosis, reduced inflammatory factors transforming growth factor (TGF) β1 (p < 0.05), IL-1β (p < 0.05) and TNF-α (p < 0.05) levels, and promoted the structural integrity of gastrocnemius and triceps muscles. Proteomics analysis demonstrated that ARC-18 treatment reversed the protein expression pattern of DMD model mice, with ATP-citrate synthase (ACLY) enriched in the TCA cycle pathway, showing a significant correlation with DMD expression levels (R = -0.72, p = 0.00031). Further investigations revealed that ARC-18 directly bound with ACLY (EC
conclusionsOur study indicated that oral ARC-18 treatment decelerated the progression of neuromuscular disease in a reliable DMD animal model, suggesting its potential as a promising drug for DMD.
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