ReviewJournal of clinical medicine2019
The "Usual Suspects": Genes for Inflammation, Fibrosis, Regeneration, and Muscle Strength Modify Duchenne Muscular Dystrophy.
Review in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.
- Predictors of cardiac disease in duchenne muscular dystrophy: a systematic review and evidence grading.Orphanet journal of rare diseases · 2024Pooled it
- Pooled it
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Navigating gastrointestinal challenges in genetic myopathies: Diagnostic insights and future directions.World journal of methodology · 2025Article
- Whole-Body Skeletal Muscle MRI Patterns in Female Dystrophinopathy Carriers.Neurology. Genetics · 2025Article
- Understanding Duchenne muscular dystrophy-associated brain pathology.Disease models & mechanisms · 2025Review
- Article
- Deletion of exons 45 to 55 in the DMD gene: from the therapeutic perspective to the in vitro model.Skeletal muscle · 2024Article
- Article
- Adults living with Duchenne muscular dystrophy: old and new challenges in a cohort of 19 patients in their third to fifth decade.European journal of neurology · 2024Article
- The complex landscape of DMD mutations: moving towards personalized medicine.Frontiers in genetics · 2024Review
- Cellular pathogenesis of Duchenne muscular dystrophy: progressive myofibre degeneration, chronic inflammation, reactive myofibrosis and satellite cell dysfunction.European journal of translational myology · 2023Article
- Association between blood eosinophil count and Duchenne muscular dystrophy severity and prognosis: a retrospective cohort study.Italian journal of pediatrics · 2023Article
- Altered muscle niche contributes to myogenic deficit in the D2-mdx model of severe DMD.Cell death discovery · 2023Article
- Is it time for genetic modifiers to predict prognosis in Duchenne muscular dystrophy?Nature reviews. Neurology · 2023Review
- A genome-wide association analysis of loss of ambulation in dystrophinopathy patients suggests multiple candidate modifiers of disease severity.European journal of human genetics : EJHG · 2023Article
- Identification of Novel Biomarkers of Spinal Muscular Atrophy and Therapeutic Response by Proteomic and Metabolomic Profiling of Human Biological Fluid Samples.Biomedicines · 2023Review
- Altered muscle niche contributes to myogenic deficit in the D2-bioRxiv : the preprint server for biology · 2023Article
- Humanization of the mdx Mouse Phenotype for Duchenne Muscular Dystrophy Modeling: A Metabolic Perspective.Journal of neuromuscular diseases · 2023Review
- Modeling Early Heterogeneous Rates of Progression in Boys with Duchenne Muscular Dystrophy.Journal of neuromuscular diseases · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD), the most severe form of dystrophinopathy, is quite homogeneous with regards to its causative biochemical defect, i.e., complete dystrophin deficiency, but not so much with regards to its phenotype. For instance, muscle weakness progresses to the loss of independent ambulation at a variable age, starting from before 10 years, to even after 16 years (with glucocorticoid treatment). Identifying the bases of such variability is relevant for patient counseling, prognosis, stratification in trials, and identification of therapeutic targets. To date, variants in five loci have been associated with variability in human DMD sub-phenotypes:
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What OpenQuestion holds
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.