ArticleThe Journal of clinical investigation2014
MicroRNA-486-dependent modulation of DOCK3/PTEN/AKT signaling pathways improves muscular dystrophy-associated symptoms.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
What it found
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Who cites it
101 citing papers in PubMed, 150 citations in OpenAlex.
- Skeletal Muscle MicroRNA Patterns in Response to a Single Bout of Exercise in Females: Biomarkers for Subsequent Training Adaptation?Biomolecules · 2023Trial
- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Candidate Circulating microRNAs in Patients with Sarcopenic Obesity: Results of a Pilot Screening.Biomedicines · 2026Article
- Modulation of miRNA networks by exercise in muscular dystrophies: therapeutic insights and future directions.Molecular and cellular biochemistry · 2026Review
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- AKT Signaling Regulates Agrin-Mediated Acetylcholine Receptor Surface Density.Medicina (Kaunas, Lithuania) · 2026Article
- Roles of microRNA in aging and dietary restriction-induced longevity.Frontiers in genetics · 2026Review
- The Potential of MicroRNAs in the Context of Sarcopenic Obesity.Physiological research · 2025Review
- Conditional Dmd ablation in muscle and brain causes profound effects on muscle function and neurobehavior.Communications biology · 2025Article
- LncRNA Xist acts as a miR-486-5p sponge to modulate myoblast proliferation by recruiting Stk4.Journal of muscle research and cell motility · 2025Article
- Local Non-Coding Regulatory Elements in Muscular Dystrophies.International journal of molecular sciences · 2025Review
- Muscle-specific increased expression ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploring lncRNA-Mediated Mechanisms in Muscle Regulation and Their Implications for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2025Review
- microRNA-133a as an indicator of disease progression and treatment response in X-linked myotubular myopathy.Molecular therapy. Nucleic acids · 2025Article
- miR-486-5p Inhibits eNOS and Angiogenesis in Cultured Endothelial Cells by Targeting MAML3.Journal of cellular and molecular medicine · 2025Article
- Circulating miRNA-486 as a novel diagnostic biomarker for right ventricular remodeling.Frontiers in cardiovascular medicine · 2025Article
- Muscle-enriched microRNA-486-mediated regulation of muscular atrophy and exercise.Journal of physiology and biochemistry · 2024Review
- Pharmacological Treatments and Therapeutic Targets in Muscle Dystrophies Generated by Alterations in Dystrophin-Associated Proteins.Medicina (Kaunas, Lithuania) · 2024Review
- Myogenic microRNAs as Therapeutic Targets for Skeletal Muscle Mass Wasting in Breast Cancer Models.International journal of molecular sciences · 2024Review
- The Role of MicroRNA in the Pathogenesis of Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024Review
41 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is caused by mutations in the gene encoding dystrophin, which results in dysfunctional signaling pathways within muscle. Previously, we identified microRNA-486 (miR-486) as a muscle-enriched microRNA that is markedly reduced in the muscles of dystrophin-deficient mice (Dmdmdx-5Cv mice) and in DMD patient muscles. Here, we determined that muscle-specific transgenic overexpression of miR-486 in muscle of Dmdmdx-5Cv mice results in reduced serum creatine kinase levels, improved sarcolemmal integrity, fewer centralized myonuclei, increased myofiber size, and improved muscle physiology and performance. Additionally, we identified dedicator of cytokinesis 3 (DOCK3) as a miR-486 target in skeletal muscle and determined that DOCK3 expression is induced in dystrophic muscles. DOCK3 overexpression in human myotubes modulated PTEN/AKT signaling, which regulates muscle hypertrophy and growth, and induced apoptosis. Furthermore, several components of the PTEN/AKT pathway were markedly modulated by miR-486 in dystrophin-deficient muscle. Skeletal muscle-specific miR-486 overexpression in Dmdmdx-5Cv animals decreased levels of DOCK3, reduced PTEN expression, and subsequently increased levels of phosphorylated AKT, which resulted in an overall beneficial effect. Together, these studies demonstrate that stable overexpression of miR-486 ameliorates the disease progression of dystrophin-deficient skeletal muscle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.