ReviewTrends in molecular medicine2016
Satellite Cells in Muscular Dystrophy - Lost in Polarity.
Review in Trends in molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
117 citing papers in PubMed.
- 4-Phenylbutyric acid activates an NF-κB-Egr-1 axis to control myoblast proliferation and ECM gene expression.iScience · 2026Article
- High-load resistance training and FSHD: harmful mixture or a silver bullet combination?Journal of neurology · 2026Review
- LKB1 Dysregulation in Duchenne Muscular Dystrophy Models: Disease Specificity and Epigenetic Control by HDAC Inhibitors.Annals of the New York Academy of Sciences · 2026Article
- Impaired Myogenic Differentiation Is a Shared Feature Across Genetic Myopathies.International journal of molecular sciences · 2026Review
- Bacteroides-derived endocannabinoid-like commendamide attenuates skeletal muscle ferroptosis in vitro: implications for Duchenne muscular dystrophy.Journal of translational medicine · 2026Article
- ANXA11 suppression restores muscular function in the mdx mouse model of Duchenne muscular dystrophy (DMD).Nature communications · 2026Article
- Gmppb-mutant mice exhibit dystroglycanopathy symptoms that are rescued with GSK3β inhibition or AAV-mediated GMPPB gene replacement.Nature communications · 2026Article
- Molecular Insights and Orthopedic Management in Muscular Dystrophies: A Comprehensive Review.International journal of molecular sciences · 2026Review
- Genetic strategies for therapy of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Review
- Myoblast paracrine factors induce catabolic remodelling in electrically stimulated myotubes.Scientific reports · 2025Article
- Article
- Cell therapy for Duchenne muscular dystrophy: promises, challenges, and controversies.Cellular and molecular life sciences : CMLS · 2025Review
- Muscle-specific increased expression ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Ubiquitination-targeted therapies improve BMD iPSC myogenic cell engraftment and dystrophin expressionMolecular therapy. Methods & clinical development · 2025Article
- Regulatory Landscapes of Muscle Satellite Cells: From Mechanism to Application.International journal of stem cells · 2025Review
- Article
- Article
- Inhibiting EZH2 complements steroid effects in Duchenne muscular dystrophy.Science advances · 2025Article
- Increased muscle satellite cell content and preserved telomere length in response to combined exercise training in patients with FSHD.The Journal of physiology · 2025Article
- Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.JCI insight · 2025Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Recent findings employing the mdx mouse model for Duchenne muscular dystrophy (DMD) have revealed that muscle satellite stem cells play a direct role in contributing to disease etiology and progression of DMD, the most common and severe form of muscular dystrophy. Lack of dystrophin expression in DMD has critical consequences in satellite cells including an inability to establish cell polarity, abrogation of asymmetric satellite stem-cell divisions, and failure to enter the myogenic program. Thus, muscle wasting in dystrophic mice is not only caused by myofiber fragility but is exacerbated by intrinsic satellite cell dysfunction leading to impaired regeneration. Despite intense research and clinical efforts, there is still no effective cure for DMD. In this review we highlight recent research advances in DMD and discuss the current state of treatment and, importantly, how we can incorporate satellite cell-targeted therapeutic strategies to correct satellite cell dysfunction in DMD.
Indexed as
Identifiers
What Socratic 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 Socratic graph.