ReviewNeuroscience letters2020
Alterations of neuromuscular junctions in Duchenne muscular dystrophy.
Review in Neuroscience letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 37 citations in OpenAlex.
- Restoration of circadian rhythm as novel targets against sarcopenia.Chinese medical journal · 2026Review
- Neuromuscular and neuromechanical assessments of respiratory performance in the mdx mouse model of Duchenne muscular dystrophy across the natural history of disease.Experimental physiology · 2026Article
- Systemic AAV9 Gene Therapy Mitigates Neuromuscular Junction Degeneration and Muscle Atrophy in a Mouse Model of CLN1 Disease.International journal of molecular sciences · 2026Article
- Assessment of muscle damage in patients with advanced Duchenne muscular dystrophy based on serum creatinine and the height-to-creatinine ratio.Frontiers in neurology · 2026Article
- When barriers fail: the role of endothelial dysfunction in rare pediatric neuromuscular diseases.Frontiers in medicine · 2026Review
- The Neuromuscular Junction: A Shared Vulnerability in Aging and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Pharmacologic Inhibition of Glutamate Dehydrogenase 1 Improves Functional Recovery of Neuromuscular Junctions and Muscle Function in Duchenne Muscular Dystrophy.The American journal of pathology · 2025Article
- Gene therapy ameliorates neuromuscular pathology in CLN3 disease.Acta neuropathologica communications · 2025Article
- Comparative Transcriptomic Profiling in Patients Affected by Duchenne and Becker Muscular Dystrophies: A Focus on ECM Genes Dysregulation.International journal of molecular sciences · 2025Article
- Dissection and Whole-Mount Immunofluorescent Staining of Mouse Hind Paw Muscles for Neuromuscular Junction Analysis.Bio-protocol · 2025Article
- Therapeutic applications and challenges in myostatin inhibition for enhanced skeletal muscle mass and functions.Molecular and cellular biochemistry · 2025Review
- Sarcoglycans are enriched at the neuromuscular junction in a nerve-dependent manner.Cell death & disease · 2025Article
- An automated platform for simultaneous, longitudinal analysis of engineered neuromuscular tissues for applications in neurotoxin potency testing.Current research in toxicology · 2025Article
- Respiratory pathology in the mdx/utrn -/- mouse: A murine model for Duchenne Muscular Dystrophy (DMD).PloS one · 2025Article
- Review
- Morphological and functional alterations of neuromuscular synapses in a mouse model of ACTA1 congenital myopathy.Human molecular genetics · 2024Article
- Accumulation of Dystrophin-Positive Muscle Fibers and Improvement of Neuromuscular Junctions in mdx Mouse Muscles after Bone Marrow Transplantation under Different Conditions.International journal of molecular sciences · 2023Article
- Mechanisms and effects of metformin on skeletal muscle disorders.Frontiers in neurology · 2023Review
- Evolution and developmental functions of the dystrophin-associated protein complex: beyond the idea of a muscle-specific cell adhesion complex.Frontiers in cell and developmental biology · 2023Review
- Early Developmental Changes of Muscle Acetylcholine Receptors Are Little Influenced by Dystrophin Absence inLife (Basel, Switzerland) · 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The focus of this review is on Duchenne muscular dystrophy (DMD), which is caused by the absence of the protein dystrophin and is characterized as a neuromuscular disease in which muscle weakness, increased susceptibility to muscle injury, and inadequate repair appear to underlie the pathology. Considerable attention has been dedicated to studying muscle fiber damage, but data show that both human patients and animal models for DMD present with fragmented neuromuscular junction (NMJ) morphology. In addition to pre- and post-synaptic abnormalities, studies indicate increased susceptibility of the NMJ to contraction-induced injury, with corresponding functional changes in neuromuscular transmission and nerve-evoked electromyographic activity. Such findings suggest that alterations in the NMJ of dystrophic muscle may play a role in muscle weakness via impairment of neuromuscular transmission. Further work is needed to fully understand the role of the NMJ in the weakness, susceptibility to injury, and progressive wasting associated with DMD.
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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.