ReviewBosnian journal of basic medical sciences2015
Dystrophin and the two related genetic diseases, Duchenne and Becker muscular dystrophies.
Review in Bosnian journal of basic medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis 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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Pooled it
- A female manifesting carrier of DMD with exon 45 deletion: a case report.Translational pediatrics · 2026Article
- Molecular Bases of Myopathies and Their Impact on Clinical Practice: Advances and Future Perspectives.International journal of molecular sciences · 2026Review
- Antisense oligonucleotides-mediated rescue of theJournal of dental sciences · 2026Article
- Ubiquitination-targeted therapies improve BMD iPSC myogenic cell engraftment and dystrophin expressionMolecular therapy. Methods & clinical development · 2025Article
- Cardiac Fibroblasts: Helping or Hurting.Genes · 2025Review
- Machine learning-based radiomics using MRI to differentiate early-stage Duchenne and Becker muscular dystrophy in children.BMC musculoskeletal disorders · 2025Article
- Dystrophinopathy in the paravertebral muscle of adolescent idiopathic scoliosis: a prospective case-control study in China.Asian spine journal · 2025Article
- Review
- Patient engagement in clinical trial design for rare neuromuscular disorders: impact on the DELIVER and ACHIEVE clinical trials.Research involvement and engagement · 2024Article
- Exploring novel natural compound-based therapies for Duchenne muscular dystrophy management: insights from network pharmacology, QSAR modeling, molecular dynamics, and free energy calculations.Frontiers in pharmacology · 2024Article
- Spirometry correlates with physical activity in patients with Duchenne muscular dystrophy.Pediatric pulmonology · 2023Article
- A novel splicing mutation identified in a DMD patient: a case report.Frontiers in pediatrics · 2023Article
- Exons 45-55 Skipping Using Antisense Oligonucleotides in Immortalized Human DMD Muscle Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Sulfur amino acid supplementation displays therapeutic potential in a C. elegans model of Duchenne muscular dystrophy.Communications biology · 2022Article
- An Ultra-Rare Manifestation of an X-Linked Recessive Disorder: Duchenne Muscular Dystrophy in a Female Patient.International journal of molecular sciences · 2022Article
- Beware of missed diagnosis in patients with multiple genetic diseases: a case report.BMC pediatrics · 2022Article
- Effects of Low-Intensity and Long-Term Aerobic Exercise on the Psoas Muscle ofInternational journal of molecular sciences · 2022Article
- Review
- Development of a model-based clinical trial simulation platform to optimize the design of clinical trials for Duchenne muscular dystrophy.CPT: pharmacometrics & systems pharmacology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations of the dystrophin DMD gene, essentially deletions of one or several exons, are the cause of two devastating and to date incurable diseases, Duchenne (DMD) and Becker (BMD) muscular dystrophies. Depending upon the preservation or not of the reading frame, dystrophin is completely absent in DMD, or present in either a mutated or a truncated form in BMD. DMD is a severe disease which leads to a premature death of the patients. Therapy approaches are evolving with the aim to transform the severe DMD in the BMD form of the disease by restoring the expression of a mutated or truncated dystrophin. These therapies are based on the assumption that BMD is a mild disease. However, this is not completely true as BMD patients are more or less severely affected and no molecular basis of this heterogeneity of the BMD form of the disease is yet understood. The aim of this review is to report for the correlation between dystrophin structures in BMD deletions in view of this heterogeneity and to emphasize that examining BMD patients in details is highly relevant to anticipate for DMD therapy effects.
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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.