ArticlePloS one2012
Agrin and synaptic laminin are required to maintain adult neuromuscular junctions.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.
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Who cites it
79 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Role of Agrin in tissue repair and regeneration: From mechanisms to therapeutic opportunities (Review).International journal of molecular medicine · 2024Pooled it
- AChRs Degeneration at NMJ in Aging-Associated Sarcopenia-A Systematic Review.Frontiers in aging neuroscience · 2020Pooled it
- Hexosamine Pathway Disruption by GFPT1 Loss Drives Coordinated Defects in Glycosylation, Autophagy, and Trafficking.Biomolecules · 2026Article
- Roles and therapeutic prospects of the laminin family in disorders of the nervous system.Journal of translational medicine · 2026Review
- Aging induces sarcopenia by disrupting the crosstalk between the skeletal muscle microenvironment and myofibers.Journal of advanced research · 2026Review
- Tongue blade neuromuscular junction defects in old F344 rats.Respiratory physiology & neurobiology · 2026Article
- Review of the Pathology of Muscle in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- SH3BP2 deficiency in skeletal muscle leads to neuromuscular junction abnormalities and decreased muscle strength.Frontiers in molecular neuroscience · 2026Article
- MuSK Regulates Neuromuscular Junction Nav1.4 Localization and Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- The extracellular matrix in peripheral nerve repair and regeneration: a narrative review of its role and therapeutic potential.Frontiers in neuroanatomy · 2025Review
- Effects of physical exercise on neuromuscular junction degeneration during ageing: A systematic review.Journal of orthopaedic translation · 2024Review
- Synergistically Acting on Myostatin and Agrin Pathways Increases Neuromuscular Junction Stability and Endurance in Old Mice.Aging and disease · 2024Article
- Skeletal muscle reprogramming enhances reinnervation after peripheral nerve injury.Research square · 2024Article
- Leveraging Biomaterial Platforms to Study Aging-Related Neural and Muscular Degeneration.Biomolecules · 2024Review
- The NDR family of kinases: essential regulators of aging.Frontiers in molecular neuroscience · 2024Review
- Multisystem physiological perspective of human frailty and its modulation by physical activity.Physiological reviews · 2023Review
- Intrafusal-fiber LRP4 for muscle spindle formation and maintenance in adult and aged animals.Nature communications · 2023Article
- Matrix produced by diseased cardiac fibroblasts affects early myotube formation and function.Acta biomaterialia · 2022Article
- SMN controls neuromuscular junction integrity through U7 snRNP.Cell reports · 2022Article
- Distinct roles of the dystrophin-glycoprotein complex: α-dystrobrevin and α-syntrophin in the maintenance of the postsynaptic apparatus of the neuromuscular synapse.Human molecular genetics · 2022Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
Funding
Abstract
As synapses form and mature the synaptic partners produce organizing molecules that regulate each other's differentiation and ensure precise apposition of pre- and post-synaptic specializations. At the skeletal neuromuscular junction (NMJ), these molecules include agrin, a nerve-derived organizer of postsynaptic differentiation, and synaptic laminins, muscle-derived organizers of presynaptic differentiation. Both become concentrated in the synaptic cleft as the NMJ develops and are retained in adulthood. Here, we used mutant mice to ask whether these organizers are also required for synaptic maintenance. Deletion of agrin from a subset of adult motor neurons resulted in the loss of acetylcholine receptors and other components of the postsynaptic apparatus and synaptic cleft. Nerve terminals also atrophied and eventually withdrew from muscle fibers. On the other hand, mice lacking the presynaptic organizer laminin-α4 retained most of the synaptic cleft components but exhibited synaptic alterations reminiscent of those observed in aged animals. Although we detected no marked decrease in laminin or agrin levels at aged NMJs, we observed alterations in the distribution and organization of these synaptic cleft components suggesting that such changes could contribute to age-related synaptic disassembly. Together, these results demonstrate that pre- and post-synaptic organizers actively function to maintain the structure and function of adult NMJs.
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Registered trials
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