ArticleResearch (Washington, D.C.)2023
Protein Arginine Methyltransferase 1 Ablation in Motor Neurons Causes Mitochondrial Dysfunction Leading to Age-related Motor Neuron Degeneration with Muscle Loss.
Article in Research (Washington, D.C.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Systematic review and meta-analysis of antioxidants with or without exercise training improving muscle condition in older adults.Scientific reports · 2025Pooled it
- Protein arginine methyltransferases as metabolic regulators: many roles beyond cancer.Science China. Life sciences · 2026Review
- Aging-Related Changes in the Injury Response of the Peripheral Nervous System.Neuroscience bulletin · 2026Review
- Protein arginine methyltransferases coordinate mitochondrial stress adaptation and neuromuscular function.Experimental & molecular medicine · 2026Review
- Pathological changes and therapeutic strategies for sarcopenia.EFORT open reviews · 2026Review
- The ageing microenvironment in sarcopenia: early alterations and targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Exercise interventions remodel the aging microenvironment to improve prognosis in older patients with cancer.Frontiers in immunology · 2026Review
- The multidimensional roles and mechanisms of exercise intervention in pediatric oncology.Frontiers in immunology · 2026Review
- Immunoinflammation and post-translational modifications in the aging process.Journal of translational medicine · 2025Review
- The protein arginine methyltransferase PRMT1 ameliorates cerebral ischemia-reperfusion injury by suppressing RIPK1-mediated necroptosis and apoptosis.Acta pharmaceutica Sinica. B · 2025Article
- Oxidative Stress in Brain Function.Antioxidants (Basel, Switzerland) · 2025Review
- PRMT5-Mediated ALKBH5 Methylation Promotes Colorectal Cancer Immune Evasion via Increasing CD276 Expression.Research (Washington, D.C.) · 2025Article
- Microdroplet-Engineered Skeletal Muscle Organoids from Primary Tissue Recapitulate Parental Physiology with High Reproducibility.Research (Washington, D.C.) · 2025Article
- Computer-assisted rehabilitation system in the use of motor function recovery: A protocol for scoping review.PloS one · 2025Article
- Regulation of dynamic spatiotemporal inflammation by nanomaterials in spinal cord injury.Journal of nanobiotechnology · 2024Review
- Review
- Advances in sarcopenia: mechanisms, therapeutic targets, and intervention strategies.Archives of pharmacal research · 2024Review
- Mitophagy Promotes Hair Regeneration by Activating Glutathione Metabolism.Research (Washington, D.C.) · 2024Article
- Fut2 Deficiency Promotes Intestinal Stem Cell Aging by Damaging Mitochondrial Functions via Down-Regulating α1,2-Fucosylation of Asah2 and Npc1.Research (Washington, D.C.) · 2024Article
- Targeted Delivery of Engineered RVG-BDNF-Exosomes: A Novel Neurobiological Approach for Ameliorating Depression and Regulating Neurogenesis.Research (Washington, D.C.) · 2024Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuromuscular dysfunction is tightly associated with muscle wasting that occurs with age or due to degenerative diseases. However, the molecular mechanisms underlying neuromuscular dysfunction are currently unclear. Recent studies have proposed important roles of Protein arginine methyltransferase 1 (Prmt1) in muscle stem cell function and muscle maintenance. In the current study, we set out to determine the role of Prmt1 in neuromuscular function by generating mice with motor neuron-specific ablation of Prmt1 (mnKO) using Hb9-Cre. mnKO exhibited age-related motor neuron degeneration and neuromuscular dysfunction leading to premature muscle loss and lethality. Prmt1 deficiency also impaired motor function recovery and muscle reinnervation after sciatic nerve injury. The transcriptome analysis of aged mnKO lumbar spinal cords revealed alterations in genes related to inflammation, cell death, oxidative stress, and mitochondria. Consistently, mnKO lumbar spinal cords of sciatic nerve injury model or aged mice exhibited elevated cellular stress response in motor neurons. Furthermore, Prmt1 inhibition in motor neurons elicited mitochondrial dysfunction. Our findings demonstrate that Prmt1 ablation in motor neurons causes age-related motor neuron degeneration attributing to muscle loss. Thus, Prmt1 is a potential target for the prevention or intervention of sarcopenia and neuromuscular dysfunction related to aging.
Identifiers
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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.