ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018
Sarcoglycan Alpha Mitigates Neuromuscular Junction Decline in Aged Mice by Stabilizing LRP4.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 3 of them syntheses that pooled it.
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Who cites it
43 citing papers in PubMed, 3 syntheses or guidelines pooled it, 61 citations in OpenAlex.
- Exploring motor unit and neuromuscular junction dysfunction in aging and sarcopenia: insights from electromyography in systematic review.GeroScience · 2026Pooled 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
- Intervening in aging and related diseases with gene therapy techniques.Cell reports. Medicine · 2026Review
- Simulated closed-loop magnetic stimulation promotes function recovery and axonal regeneration in spinal cord injury.Communications biology · 2026Article
- Dietary nitrate supplementation mitigates age-related changes at the neuromuscular junction in mice.The Journal of physiology · 2026Article
- Repairing the defective folding of alpha-sarcoglycan is needed to promote myogenic cell engraftment in 3D artificial muscle models of LGMDR3.Skeletal muscle · 2025Article
- Neural Cues and Genomic Clues: NGS Insights into Neurogenic Sarcopenia and Muscle Atrophy.International journal of molecular sciences · 2025Review
- Sarcoglycans are enriched at the neuromuscular junction in a nerve-dependent manner.Cell death & disease · 2025Article
- Alterations in neuromuscular junction morphology with ageing and endurance training modulate neuromuscular transmission and myofibre composition.The Journal of physiology · 2025Article
- Free essential amino acid feeding improves endurance during resistance training via DRP1-dependent mitochondrial remodelling.Journal of cachexia, sarcopenia and muscle · 2024Article
- The MuSK agonist antibody protects the neuromuscular junction and extends the lifespan in C9orf72-ALS mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Neuronal LRP4 directs the development, maturation and cytoskeletal organization of Drosophila peripheral synapses.Development (Cambridge, England) · 2024Article
- Building, Breaking, and Repairing Neuromuscular Synapses.Cold Spring Harbor perspectives in biology · 2024Review
- Disruption of Neuromuscular Junction Following Spinal Cord Injury and Motor Neuron Diseases.International journal of molecular sciences · 2024Review
- Deficiency of skeletal muscle Agrin contributes to the pathogenesis of age-related sarcopenia in mice.Cell death & disease · 2024Article
- Calcium-binding protein 7 expressed in muscle negatively regulates age-related degeneration of neuromuscular junctions in mice.iScience · 2024Article
- Dual electrical stimulation at spinal-muscular interface reconstructs spinal sensorimotor circuits after spinal cord injury.Nature communications · 2024Article
- Long-term muscle-specific overexpression of DOK7 in mice using AAV9-tMCK-DOK7.Molecular therapy. Nucleic acids · 2023Article
- Older mice show decreased regeneration of neuromuscular junctions following lengthening contraction-induced injury.GeroScience · 2023Article
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 3 countries.
Funding
Abstract
During aging, acetylcholine receptor (AChR) clusters become fragmented and denervated at the neuromuscular junction (NMJ). Underpinning molecular mechanisms are not well understood. We showed that LRP4, a receptor for agrin and critical for NMJ formation and maintenance, was reduced at protein level in aged mice, which was associated with decreased MuSK tyrosine phosphorylation, suggesting compromised agrin-LRP4-MuSK signaling in aged muscles. Transgenic expression of LRP4 in muscles alleviated AChR fragmentation and denervation and improved neuromuscular transmission in aged mice. LRP4 ubiquitination was augmented in aged muscles, suggesting increased LRP4 degradation as a mechanism for reduced LRP4. We found that sarcoglycan α (SGα) interacted with LRP4 and delayed LRP4 degradation in cotransfected cells. AAV9-mediated expression of SGα in muscles mitigated AChR fragmentation and denervation and improved neuromuscular transmission in aged mice. These observations support a model where compromised agrin-LRP4-MuSK signaling serves as a pathological mechanism of age-related NMJ decline and identify a novel function of SGα in stabilizing LRP4 for NMJ stability in aged mice.
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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.