ReviewFrontiers in aging neuroscience2014
Degeneration of neuromuscular junction in age and dystrophy.
Review in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 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
120 citing papers in PubMed, 1 synthesis or guideline pooled it.
- AChRs Degeneration at NMJ in Aging-Associated Sarcopenia-A Systematic Review.Frontiers in aging neuroscience · 2020Pooled it
- The Motor Neuromuscular Axis: The Overlooked Element of Developmental Programming in Diabetes and Metabolic Syndrome.International journal of molecular sciences · 2026Review
- Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Lysophosphatidic acid mediates skeletal muscle fibrosis in denervation via activation of YAP/TAZ.JCI insight · 2026Article
- Article
- The Role of Polyphenols in Regulating Skeletal Muscle Development and Homeostasis: Molecular Mechanisms and Potential Medical Applications.Molecular nutrition & food research · 2026Review
- Changes in the Structure of the Neuromuscular Junction and Muscle Fiber Types Following an Acute Injury Model Induced by Eccentric Contraction.Current issues in molecular biology · 2026Article
- Anti-Inflammatory and Synaptic Protective Effects of TNF-α Inactivation in the MDX Mouse Model.Current issues in molecular biology · 2026Article
- Spatiotemporal Remodeling of Presynaptic Terminals in Human Neuromuscular Junctions.International journal of molecular sciences · 2026Article
- A Validated Transcriptomic NMJ Remodeling Score Reveals Synaptic Dysfunction Independent of Muscle Atrophy after Immobilization in a Microgravity Analog.Neuroinformatics · 2026Article
- Myasthenia gravis: from recognition of heterogeneity to a paradigm shift toward precision therapy.Frontiers in immunology · 2026Review
- Tendon-muscle-nerve disconnection in chronic large and massive posterosuperior rotator cuff tears: a targeted narrative mechanistic review and hypothesis-generating framework.Frontiers in cell and developmental biology · 2026Review
- Dietary nitrate supplementation mitigates age-related changes at the neuromuscular junction in mice.The Journal of physiology · 2026Article
- Sarcopenia in the Aging Process: Pathophysiological Mechanisms, Clinical Implications, and Emerging Therapeutic Approaches.International journal of molecular sciences · 2025Review
- A role for the transcriptional coregulator RIP140 in the control of muscle endurance fitness.JCI insight · 2025Article
- New Insights into Potential Anti-Aging and Fatigue Effects of a Dietary Supplement from the Resveratrol Beverage in Aged SAMP8 Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Review
- Expansion microscopy reveals nano-scale insights into the human neuromuscular junction.Cell reports methods · 2025Article
- MuSK Regulates Neuromuscular Junction Nav1.4 Localization and Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Macrophages producing chondroitin sulfate proteoglycan-4 induce neuro-cardiac junction impairment in Duchenne muscular dystrophy.The Journal of pathology · 2025Article
60 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
4 authors.
Funding
Abstract
Functional denervation is a hallmark of aging sarcopenia as well as of muscular dystrophy. It is thought to be a major factor reducing skeletal muscle mass, particularly in the case of sarcopenia. Neuromuscular junctions (NMJs) serve as the interface between the nervous and skeletal muscular systems, and thus they may receive pathophysiological input of both pre- and post-synaptic origin. Consequently, NMJs are good indicators of motor health on a systemic level. Indeed, upon sarcopenia and dystrophy, NMJs morphologically deteriorate and exhibit altered characteristics of primary signaling molecules, such as nicotinic acetylcholine receptor and agrin. Since a remarkable reversibility of these changes can be observed by exercise, there is significant interest in understanding the molecular mechanisms underlying synaptic deterioration upon aging and dystrophy and how synapses are reset by the aforementioned treatments. Here, we review the literature that describes the phenomena observed at the NMJ in sarcopenic and dystrophic muscle as well as to how these alterations can be reversed and to what extent. In a second part, the current information about molecular machineries underlying these processes is reported.
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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.