ReviewFundamental research2022
Promising therapeutic approaches of utrophin replacing dystrophin in the treatment of Duchenne muscular dystrophy.
Review in Fundamental research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Magnetic Mitohormesis as a Potential Non-Invasive Restorative Therapy for X-Linked Muscular Dystrophies.International journal of molecular sciences · 2026Review
- Bridging Duchenne muscular dystrophy therapy from rhesus monkeys to patients.Clinical and translational medicine · 2026Article
- Low-dose MyoAAV 2A-mediated delivery of engineered micro-utrophin achieves pan- muscle tissue distribution with elevated muscle function in Duchenne muscular dystrophy.Journal of translational medicine · 2026Article
- Myotendinous Junction development and repair.Journal of orthopaedic translation · 2026Review
- (Z)-Endoxifen as a Potential Modulator of Utrophin Pathways in Duchenne Muscular Dystrophy: A Mechanistic and Transcriptomic Perspective.Degenerative neurological and neuromuscular disease · 2026Review
- Systemic MyoAAV-saRNA delivery activates endogenous utrophin and rescues dystrophic pathology in mdx mice.Regenerative therapy · 2025Article
- AI-driven discovery of novel extracellular matrix biomarkers in pelvic organ prolapse.PLoS computational biology · 2025Article
- Machine-guided dual-objective protein engineering for deimmunization and therapeutic functions.Cell systems · 2025Article
- Activation of endogenous full-length utrophin by MyoAAV-UA as a therapeutic approach for Duchenne muscular dystrophy.Nature communications · 2025Article
- Gene therapy delivered micro-dystrophins co-localize with transgenic utrophin in dystrophic skeletal muscle fibers.Neuromuscular disorders : NMD · 2024Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is a serious genetic neuromuscular rare disease that is prevalent and caused by the mutation/deletion of the X-linked DMD gene that encodes dystrophin. Utrophin is a dystrophin homologous protein on human chromosome 6. Dystrophin and utrophin are highly homologous. They can recruit many dystrophin-glycoprotein complex (DGC)-related proteins and co-localize at the sarcolemma in the early stage of human embryonic development. Moreover, utrophin is overexpressed naturally at the mature myofiber sarcolemma in DMD patients. Therefore, utrophin is considered the most promising homologous protein to replace dystrophin. This review summarizes various modulating drugs and gene therapy approaches for utrophin replacement. As a universal method to treat DMD disease, utrophin has a promising therapeutic prospect and deserves further investigation.
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