ArticleJCI insight2020
Lack of miR-378 attenuates muscular dystrophy in mdx mice.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.
- Prognostic significance of miR-378 in cancers: a meta-analysis.BMC cancer · 2025Pooled it
- Muscle and cardiac therapeutic strategies for Duchenne muscular dystrophy: past, present, and future.Pharmacological reports : PR · 2020Pooled it
- Small Extracellular Vesicle Release Following Electrical Pulse Stimulation of C2C12 Myotubes: Effects on microRNA Cargo and Myoblast Migration and Differentiation.International journal of molecular sciences · 2026Article
- [Advances in the role of miR-378a in skeletal muscle development and diseases].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Review
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Genetic strategies for therapy of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Review
- MicroRNA-33 inhibition ameliorates muscular dystrophy by enhancing skeletal muscle regeneration.EMBO molecular medicine · 2025Article
- FNDC1 is a myokine that promotes myogenesis and muscle regeneration.The EMBO journal · 2025Article
- Origins and functions of eosinophils in two non-mucosal tissues.Frontiers in immunology · 2024Review
- Compromised diabetic heart function is not affected by miR-378a upregulation upon hyperglycemia.Pharmacological reports : PR · 2023Article
- miR-378 influences muscle satellite cells and enhances adipogenic potential of fibro-adipogenic progenitors but does not affect muscle regeneration in the glycerol-induced injury model.Scientific reports · 2023Article
- A cellular and molecular spatial atlas of dystrophic muscle.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- MicroRNA as potential biomarker for severity, progression, and therapeutic monitoring in animal models of limb-girdle muscular dystrophy: a systematic review.Frontiers in cellular neuroscience · 2023Review
- Histological Methods to Assess Skeletal Muscle Degeneration and Regeneration in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2022Review
- Article
- miR-491-5p inhibits Emilin 1 to promote fibroblasts proliferation and fibrosis in gluteal muscle contracture via TGF-Beta1/Smad2 pathway.Physiological research · 2022Article
- Gestational Exercise Increases Male Offspring's Maximal Workload Capacity Early in Life.International journal of molecular sciences · 2022Article
- Dysregulated Autophagy and Mitophagy in a Mouse Model of Duchenne Muscular Dystrophy Remain Unchanged Following Heme Oxygenase-1 Knockout.International journal of molecular sciences · 2021Article
- Simvastatin does not alleviate muscle pathology in a mouse model of Duchenne muscular dystrophy.Skeletal muscle · 2021Article
- Cellular pathology of the human heart in Duchenne muscular dystrophy (DMD): lessons learned from in vitro modeling.Pflugers Archiv : European journal of physiology · 2021Review
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The severity of Duchenne muscular dystrophy (DMD), an incurable disease caused by the lack of dystrophin, might be modulated by different factors, including miRNAs. Among them, miR-378 is considered of high importance for muscle biology, but intriguingly, its role in DMD and its murine model (mdx mice) has not been thoroughly addressed so far. Here, we demonstrate that dystrophic mice additionally globally lacking miR-378 (double-KO [dKO] animals) exhibited better physical performance and improved absolute muscle force compared with mdx mice. Accordingly, markers of muscle damage in serum were significantly decreased in dKO mice, accompanied by diminished inflammation, fibrosis, and reduced abundance of regenerating fibers within muscles. The lack of miR-378 also normalized the aggravated fusion of dystrophin-deficient muscle satellite cells (mSCs). RNA sequencing of gastrocnemius muscle transcriptome revealed fibroblast growth factor 1 (Fgf1) as one of the most significantly downregulated genes in mice devoid of miR-378, indicating FGF1 as one of the mediators of changes driven by the lack of miR-378. In conclusion, we suggest that targeting miR-378 has the potential to ameliorate DMD pathology.
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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.