ArticleJCI insight2017
MicroRNA-29 overexpression by adeno-associated virus suppresses fibrosis and restores muscle function in combination with micro-dystrophin.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Transforming Duchenne muscular dystrophy therapy: The multifaceted role of extracellular vesicles and exosomes.Biochemistry and biophysics reports · 2026Review
- Disease exacerbation in human DMD MYOrganoids enables gene therapy evaluation and unveils persistence of fibrotic activity.NPJ Regenerative medicine · 2026Article
- Genetic strategies for therapy of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Review
- Intraperitoneal administration of adeno-associated virus encoding microRNA-29b for the treatment of peritoneal metastasis.Cancer gene therapy · 2024Article
- Advances in non-coding RNA in tendon injuries.Frontiers in genetics · 2024Review
- Putting the "mi" in omics: discovering miRNA biomarkers for pediatric precision care.Pediatric research · 2023Review
- Nintedanib Reduces Muscle Fibrosis and Improves Muscle Function of the Alpha-Sarcoglycan-Deficient Mice.Biomedicines · 2022Article
- MicroRNAs in Dystrophinopathy.International journal of molecular sciences · 2022Review
- miR-491-5p inhibits Emilin 1 to promote fibroblasts proliferation and fibrosis in gluteal muscle contracture via TGF-Beta1/Smad2 pathway.Physiological research · 2022Article
- Review
- MiRNAs and Muscle Regeneration: Therapeutic Targets in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2021Review
- Noncoding RNAs in Duchenne and Becker muscular dystrophies: role in pathogenesis and future prognostic and therapeutic perspectives.Cellular and molecular life sciences : CMLS · 2020Review
- MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy.Cardiovascular diabetology · 2020Review
- Age-Associated Salivary MicroRNA Biomarkers for Oculopharyngeal Muscular Dystrophy.International journal of molecular sciences · 2020Article
- miR-29a is a potential protective factor for fibrogenesis in gluteal muscle contracture.Physiological research · 2020Article
- miR-381 Attenuates Peripheral Neuropathic Phenotype Caused by Overexpression of PMP22.Experimental neurobiology · 2019Article
- Expanding the horizons of microRNA bioinformatics.RNA (New York, N.Y.) · 2018Article
- Generation of MicroRNA-34 Sponges and Tough Decoys for the Heart: Developments and Challenges.Frontiers in pharmacology · 2018Article
- Combined Therapies for Duchenne Muscular Dystrophy to Optimize Treatment Efficacy.Frontiers in genetics · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is caused by dystrophin deficiency resulting in progressive muscle weakness and fibrotic scarring. Muscle fibrosis impairs blood flow, hampering muscle repair and regeneration. Irrespective of the success of gene restoration, functional improvement is limited without reducing fibrosis. The levels of miR-29c, a known regulator of collagen, are reduced in DMD. Our goal is to develop translational, antifibrotic therapy by overexpressing miR-29c. We injected the gastrocnemius muscle with either self-complementary AAV.CMV.miR-29c or single-stranded AAV.MCK.micro-dystrophin alone or in combination in the mdx/utrn+/- mouse, a DMD mouse model. Treatment of 3-month-old mdx/utrn+/- mice with AAV.miR-29c showed a reduction in collagen and increased absolute and specific force compared with untreated animals, but neither parameter reached WT levels. Combinatorial gene delivery in 3-month-old mdx/utrn+/- mice further decreased fibrosis, and showed a reduction of transcript levels for Col1A, Col3A, fibronectin, and Tgfb1. In addition, absolute and specific force was normalized and equivalent to WT. However, protection against eccentric contraction fell short of WT levels at this time point. When this same mouse model was treated with miR-29c/micro-dystrophin combinatorial therapy at 1 month of age, there was complete normalization of specific and absolute force and protection against eccentric contraction-induced injury was comparable to WT. These findings highlight the potential for miR-29c as an important addition to the armamentarium for translational gene therapy, especially when used in combination with micro-dystrophin in DMD.
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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.