ArticleJournal of cachexia, sarcopenia and muscle2025
Oestrogen Receptor Alpha in Myocyte Maintains Muscle Regeneration in 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 2 papers.
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2 citing papers in PubMed.
- Lycopene Increases Skeletal Muscle Mass by Promoting Myoblast Differentiation.Food science & nutrition · 2026Article
- Tumor-derived MG53 aggravates gastrointestinal cancer cachexia related muscle atrophy by inhibiting the TLR4/PI3K/AKT/FOXO3a signaling pathway.Frontiers in oncology · 2026Article
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13 authors.
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Abstract
backgroundOestrogen receptor alpha (ERα) plays an important role in maintaining mitochondrial function and regulating metabolism in skeletal muscle. However, its alterations and potential mechanisms in Duchenne muscular dystrophy (DMD) remain incompletely understood. In this study, we demonstrated the protective role of ERα in myocyte for skeletal muscle regeneration in mdx mice and explored the therapeutic effects of oestrogen receptor modulators on DMD.
methodsDMD patients' biopsies were obtained for histological analysis to explore the expression of ERα. The phenotype of muscle was analysed by histology and molecular biology. The therapeutical effect of different oestrogen receptor modulators was examined in mdx mice treated with fulvestrant (FVT, 20 mg/kg once a week) or oestradiol (E2, 1 mg/kg per day) for 4 weeks. The protective effect of ERα was performed on mdx mice after conditional knockout of ERα in skeletal muscle (ERα
resultsThe ERα expression was increased in DMD patients' triceps (p < 0.05) and mdx mice muscles (p < 0.05). FVT reduced ERα levels in the mdx mice muscles (p < 0.01) but had no significant effect on skeletal muscle regeneration on mdx mice. Compared with mdx mice, E2 reduced the levels of creatine kinase (CK) and lactic dehydrogenase (LDH) (p < 0.001) in serum, enhanced skeletal muscle function, alleviated skeletal muscle atrophy and fibre loss and upregulated the expression of ERα in GAS (p < 0.001) and TA (p < 0.05). The myogenic factors such as myosin heavy chain (MyHC, p < 0.001), myogenin (MyoG, p < 0.05), MyoD (p < 0.05) and ERRα (p < 0.001) were increased in mdx mice GAS with E2. But E2 had no effect on ERα
conclusionWe demonstrated that ERα in myocyte exerted a protective effect on skeletal muscle regeneration in DMD patients and mdx mice through the ERα-ERRα-MyoD pathway, which has potential implications for DMD therapy strategies.
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