ReviewInternational journal of molecular sciences2024
The Role of MicroRNA in the Pathogenesis of Duchenne Muscular Dystrophy.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The role of non-coding RNAs in the coronary no-reflow phenomenon: a systematic review.Molecular biology reports · 2026Pooled it
- The Role of MicroRNAs in Progressive Supranuclear Palsy-A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Modulation of miRNA networks by exercise in muscular dystrophies: therapeutic insights and future directions.Molecular and cellular biochemistry · 2026Review
- Plasma Micro-RNA Signatures of Type 1 Ryanodine Receptor Related Myopathies.bioRxiv : the preprint server for biology · 2026Article
- MicroRNA Regulatory Targets Related to VObioRxiv : the preprint server for biology · 2026Article
- The miR-30c-5p/SOCS3 axis is a potential driver of inflammation and metabolic imbalance in Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2026Article
- MicroRNA signatures of cardiorespiratory fitness (VO2peak) in older adults: Insights from the study of muscle, mobility, and aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- MyomiRs Expression in Limb Girdle Muscular Dystrophy.IUBMB life · 2025Review
- miR-33 inhibition as a novel therapeutic approach for treating muscular dystrophy.EMBO molecular medicine · 2025Article
- Regulating the expression of exercise-induced micro-RNAs and long non-coding RNAs: implications for controlling cardiovascular diseases and heart failure.Frontiers in molecular biosciences · 2025Review
- The Role of Alarmins in the Pathogenesis of Atherosclerosis and Myocardial Infarction.Current issues in molecular biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked progressive disorder associated with muscle wasting and degeneration. The disease is caused by mutations in the gene that encodes dystrophin, a protein that links the cytoskeleton with cell membrane proteins. The current treatment methods aim to relieve the symptoms of the disease or partially rescue muscle functionality. However, they are insufficient to suppress disease progression. In recent years, studies have uncovered an important role for non-coding RNAs (ncRNAs) in regulating the progression of numerous diseases. ncRNAs, such as micro-RNAs (miRNAs), bind to their target messenger RNAs (mRNAs) to suppress translation. Understanding the mechanisms involving dysregulated miRNAs can improve diagnosis and suggest novel treatment methods for patients with DMD. This review presents the available evidence on the role of altered expression of miRNAs in the pathogenesis of DMD. We discuss the involvement of these molecules in the processes associated with muscle physiology and DMD-associated cardiomyopathy.
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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.