ArticleeNeuro
Semaphorin3A Signaling Is Dispensable for Motor Axon Reinnervation of the Adult Neuromuscular Junction.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Conserved differential expression of DDX helicase and CPEB genes in skeletal muscles potentially influences neuromuscular junctions during aging: a computational analysis.Biogerontology · 2026Article
- Deletion of murineScience translational medicine · 2025Article
- A unifying mechanism for presynaptic homeostatic plasticity at mammalian peripheral and central synapses.Neuron · 2025Article
- Semaphorins: Missing Signals in Age-dependent Alteration of Neuromuscular Junctions and Skeletal Muscle Regeneration.Aging and disease · 2024Review
- DLK signaling in axotomized neurons triggers complement activation and loss of upstream synapses.Cell reports · 2024Article
- Transcriptome profiling of a synergistic volumetric muscle loss repair strategy.BMC musculoskeletal disorders · 2023Article
- Increased Epidermal Nerve Growth Factor without Small-Fiber Neuropathy in Dermatomyositis.International journal of molecular sciences · 2022Article
- Modelling and Refining Neuronal Circuits with Guidance Cues: Involvement of Semaphorins.International journal of molecular sciences · 2021Review
- miR-30b Promotes spinal cord sensory function recovery via the Sema3A/NRP-1/PlexinA1/RhoA/ROCK Pathway.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The neuromuscular junction (NMJ) is a specialized synapse that is formed by motor axon innervation of skeletal muscle fibers. The maintenance of motor-muscle connectivity is critical for the preservation of muscle tone and generation of movement. Injury can induce a robust regenerative response in motor axons, but severe trauma or chronic denervation resulting from neurodegenerative disease typically leads to inefficient repair and poor functional recovery. The axon guidance molecule Semaphorin3A (Sema3A) has been implicated as a negative regulator of motor innervation. Upon binding to a plexinA-neuropilin1 (Npn1) receptor complex, Sema3A initiates a downstream signaling cascade that results in axonal repulsion. Here, we established a reproducible nerve crush model to quantify motor nerve regeneration. We then used that model to investigate the role of Sema3A signaling at the adult NMJ. In contrast to previous findings, we found that
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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.