ArticleScientific reports2020
miR-379 links glucocorticoid treatment with mitochondrial response in Duchenne muscular dystrophy.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 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.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Lysosomal damage is a therapeutic target in Duchenne muscular dystrophy.Science advances · 2025Article
- Mitochondrial dysfunction as a key player in aggravating periodontitis among diabetic patients: review of the current scope of knowledge.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Label-free proteomic analysis of Duchenne and Becker muscular dystrophy showed decreased sarcomere proteins and increased ubiquitination-related proteins.Scientific reports · 2025Article
- miR-379-5p retards the proliferation and differentiation of goat skeletal muscle satellite cells by targetingFrontiers in veterinary science · 2025Article
- Effects of Low and High Maternal Protein Intake on Fetal Skeletal Muscle miRNAome in Sheep.Animals : an open access journal from MDPI · 2024Article
- MicroRNA-877-5p promotes osteoblast differentiation by targeting EIF4G2 expression.Journal of orthopaedic surgery and research · 2024Article
- Identification of reference microRNAs in skeletal muscle of a canine model of Duchenne muscular dystrophy.Wellcome open research · 2024Article
- Article
- 2023 Padua Days of Muscle and Mobility Medicine: post-meeting Book of Abstracts.European journal of translational myology · 2023Article
- Specific mechanisms of translation initiation in higher eukaryotes: the eIF4G2 story.RNA (New York, N.Y.) · 2023Review
- Abstracts of the 2023 Padua Days of Muscle and Mobility Medicine (2023Pdm3) to be held March 29 - April 1 at the Galileian Academy of Padua and at the Petrarca Hotel, Thermae of Euganean Hills, Padua, Italy.European journal of translational myology · 2023Article
- Dlk1-Dio3 cluster miRNAs regulate mitochondrial functions in the dystrophic muscle in Duchenne muscular dystrophy.Life science alliance · 2023Article
- Deciphering the Molecular Mechanism of Incurable Muscle Disease by a Novel Method for the Interpretation of miRNA Dysregulation.Non-coding RNA · 2022Article
- A revised model for mitochondrial dysfunction in Duchenne muscular dystrophy.European journal of translational myology · 2021Article
- Cholesterol metabolism is a potential therapeutic target in Duchenne muscular dystrophy.Journal of cachexia, sarcopenia and muscle · 2021Article
- Translational research on Myology and Mobility Medicine: 2021 semi-virtual PDM3 from Thermae of Euganean Hills, May 26 - 29, 2021.European journal of translational myology · 2021Article
- 30 Years of Translational Mobility Medicine: 2020 Padua Muscle Days go virtual from Euganean Hills, November 19th to 21st.European journal of translational myology · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne Muscular Dystrophy (DMD) is a lethal muscle disorder, caused by mutations in the DMD gene and affects approximately 1:5000-6000 male births. In this report, we identified dysregulation of members of the Dlk1-Dio3 miRNA cluster in muscle biopsies of the GRMD dog model. Of these, we selected miR-379 for a detailed investigation because its expression is high in the muscle, and is known to be responsive to glucocorticoid, a class of anti-inflammatory drugs commonly used in DMD patients. Bioinformatics analysis predicts that miR-379 targets EIF4G2, a translational factor, which is involved in the control of mitochondrial metabolic maturation. We confirmed in myoblasts that EIF4G2 is a direct target of miR-379, and identified the DAPIT mitochondrial protein as a translational target of EIF4G2. Knocking down DAPIT in skeletal myotubes resulted in reduced ATP synthesis and myogenic differentiation. We also demonstrated that this pathway is GC-responsive since treating mice with dexamethasone resulted in reduced muscle expression of miR-379 and increased expression of EIF4G2 and DAPIT. Furthermore, miR-379 seric level, which is also elevated in the plasma of DMD patients in comparison with age-matched controls, is reduced by GC treatment. Thus, this newly identified pathway may link GC treatment to a mitochondrial response 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 Socratic graph.