ArticleRare diseases (Austin, Tex.)2014
Muscle-specific microRNAs as biomarkers of Duchenne Muscular Dystrophy progression and response to therapies.
Article in Rare diseases (Austin, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03319030 (Evaluating the Impact of Aerobic Exercise in Boys With Duchenne Muscular Dystrophy), which is not on this map. Cited by 11 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Evaluating the Impact of Aerobic Exercise in Boys With Duchenne Muscular Dystrophy (DMD)
Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- PdgfrαGenes & diseases · 2025Review
- MicroRNAs as a Tool for Differential Diagnosis of Neuromuscular Disorders.Neuromolecular medicine · 2023Article
- Histone Deacetylases: Molecular Mechanisms and Therapeutic Implications for Muscular Dystrophies.International journal of molecular sciences · 2023Review
- Non-coding RNAs in human health and disease: potential function as biomarkers and therapeutic targets.Functional & integrative genomics · 2023Review
- Non-myogenic mesenchymal cells contribute to muscle degeneration in facioscapulohumeral muscular dystrophy patients.Cell death & disease · 2022Article
- The pan HDAC inhibitor Givinostat improves muscle function and histological parameters in two Duchenne muscular dystrophy murine models expressing different haplotypes of the LTBP4 gene.Skeletal muscle · 2021Article
- Rotator cuff tear degeneration and the role of fibro-adipogenic progenitors.Annals of the New York Academy of 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
- Peptide-conjugate antisense based splice-correction for Duchenne muscular dystrophy and other neuromuscular diseases.EBioMedicine · 2019Review
- MicroRNAs and Long Non-coding RNAs in Genetic Diseases.Molecular diagnosis & therapy · 2019Review
- Epigenetic Reprogramming of Muscle Progenitors: Inspiration for Clinical Therapies.Stem cells international · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have revealed the contribution of fibro-adipogenic progenitors (FAPs) to the pathogenesis and progression of Duchenne Muscular Dystrophy (DMD). While FAPs direct compensatory regeneration at early stages of disease, as the disease progresses they contribute to the progressive replacement of contractile myofibers with fibrotic scars and fatty infiltration. Using the mouse model of DMD - the mdx mice - we have recently reported that FAPs mediate the ability of HDAC inhibitors (HDACi) to promote muscle regeneration and prevent fibro-adipogenic degeneration at early stages of disease. This effect is mediated by the induction of myomiRs that, in turn, target the SWI/SNF components BAF60A and B, thereby favoring the formation of BAF60C-based SWI/SNF complex, which directs the switch from the fibro-adipogenic to the myogenic lineage. Here we show direct evidence of induction of miR-206 and BAF60C, and reduction of BAF60A, in FAPs isolated from mdx muscles exposed to the HDACi Trichostatin A (TSA). We also discuss how increased expression of myomiRs in dystrophic muscles can be integrated with circulating myomiRs to provide accurate biomarkers of disease progression and response to treatment.
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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.