ArticlePloS one2018
Cycles of myofiber degeneration and regeneration lead to remodeling of the neuromuscular junction in two mammalian models of Duchenne muscular dystrophy.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 52 citations in OpenAlex.
- The perijunctional zone is a molecularly distinct muscle subdomain altered in Duchenne muscular dystrophy.Nature communications · 2026Article
- Early postsynaptic instability and acetylcholine receptor compartmentalization precede neuromuscular synapse dismantling.Communications biology · 2026Article
- New Insights into Neuromuscular Junction Biology: Evidence from Human and Animal Research.International journal of molecular sciences · 2026Review
- Identification of CaVβ1 Isoforms Required for Neuromuscular Junction Formation and Maintenance.Cells · 2025Article
- 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
- Long-Term Engraftment and Satellite Cell Expansion from Human PSC Teratoma-Derived Myogenic Progenitors.Cells · 2025Article
- MuSK Regulates Neuromuscular Junction Nav1.4 Localization and Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Origin, identity, and function of terminal Schwann cells.Trends in neurosciences · 2024Review
- Morphological and functional alterations of neuromuscular synapses in a mouse model of ACTA1 congenital myopathy.Human molecular genetics · 2024Article
- Cellular and molecular evidence that synaptic Schwann cells contribute to aging of mouse neuromuscular junctions.Aging cell · 2023Article
- 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
- Maintenance of subsynaptic myonuclei number is not driven by neural input.Frontiers in physiology · 2023Article
- Histological Methods to Assess Skeletal Muscle Degeneration and Regeneration in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2022Review
- Early Developmental Changes of Muscle Acetylcholine Receptors Are Little Influenced by Dystrophin Absence inLife (Basel, Switzerland) · 2022Article
- Balanced Free Essential Amino Acids and Resistance Exercise Training Synergistically Improve Dexamethasone-Induced Impairments in Muscle Strength, Endurance, and Insulin Sensitivity in Mice.International journal of molecular sciences · 2022Article
- Muscle Damage in Dystrophic mdx Mice Is Influenced by the Activity of CaLife (Basel, Switzerland) · 2022Article
- KMT5B is required for early motor development.Frontiers in genetics · 2022Article
- Lithium causes differential effects on postsynaptic stability in normal and denervated neuromuscular synapses.Scientific reports · 2021Article
- Catalpol counteracts the pathology in a mouse model of Duchenne muscular dystrophy by inhibiting the TGF-β1/TAK1 signaling pathway.Acta pharmacologica Sinica · 2021Article
- Myogenesis modelled by human pluripotent stem cells: a multi-omic study of Duchenne myopathy early onset.Journal of cachexia, sarcopenia and muscle · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mice lacking the sarcolemmal protein dystrophin, designated mdx, have been widely used as a model of Duchenne muscular dystrophy. Dystrophic mdx mice as they mature develop notable morphological abnormalities to their neuromuscular junctions, the peripheral cholinergic synapses responsible for activating muscle fibers. Most obviously the acetylcholine receptor aggregates are fragmented into small non-continuous, islands. This contrasts with wild type mice whose acetylcholine receptor aggregates are continuous and pretzel-shaped in appearance. We show here that these abnormalities in mdx mice are also present in a canine model of Duchenne muscular dystrophy and provide additional evidence to support the hypothesis that NMJ remodeling occurs due to myofiber degeneration and regeneration. Using a method to investigate synaptic AChR replacement, we show that neuromuscular junction remodeling in mdx animals is caused by muscle fiber degeneration and regeneration at the synaptic site and is mimicked by deliberate myofiber injury in wild type mice. Importantly, the innervating motor axon plays a crucial role in directing the remodeling of the neuromuscular junction in dystrophy, as has been recorded in aging and deliberate muscle fiber injury in wild type mice. The remodeling occurs repetitively through the life of the animal and the changes in junctions become greater with age.
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