ArticleThe American journal of pathology1999
Hindlimb motor neurons require Cu/Zn superoxide dismutase for maintenance of neuromuscular junctions.
Article in The American journal of pathology, 1999. 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, 99 citations in OpenAlex.
- CTRP10 is required for optimal motor function.The Journal of biological chemistry · 2026Article
- Mouse models used to test the role of reactive oxygen species in aging and age-related chronic diseases.Free radical biology & medicine · 2024Review
- Protein aggregation and therapeutic strategies in SOD1- and TDP-43- linked ALS.Frontiers in molecular biosciences · 2024Review
- AAV1.NT-3 gene therapy in the SOD1KO mouse model of accelerated sarcopenia.Journal of cachexia, sarcopenia and muscle · 2023Article
- Mitochondrial Dysfunction in Intensive Care Unit-Acquired Weakness and Critical Illness Myopathy: A Narrative Review.International journal of molecular sciences · 2023Review
- Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic.Angewandte Chemie (International ed. in English) · 2021Review
- Review
- Impairment Mechanisms and Intervention Approaches for Aged Human Neuromuscular Junctions.Frontiers in molecular neuroscience · 2020Review
- Single copy/knock-in models of ALS SOD1 in C. elegans suggest loss and gain of function have different contributions to cholinergic and glutamatergic neurodegeneration.PLoS genetics · 2018Article
- Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling.The Journal of cell biology · 2018Review
- Role of nerve-muscle interactions and reactive oxygen species in regulation of muscle proteostasis with ageing.The Journal of physiology · 2017Review
- Effects of Aging and Oxidative Stress on Spermatozoa of Superoxide-Dismutase 1- and Catalase-Null Mice.Biology of reproduction · 2016Article
- The Role of Autophagy, Mitophagy and Lysosomal Functions in Modulating Bioenergetics and Survival in the Context of Redox and Proteotoxic Damage: Implications for Neurodegenerative Diseases.Aging and disease · 2016Review
- Mechanisms of Muscle Denervation in Aging: Insights from a Mouse Model of Amyotrophic Lateral Sclerosis.Aging and disease · 2015Review
- A novel SOD1-ALS mutation separates central and peripheral effects of mutant SOD1 toxicity.Human molecular genetics · 2015Article
- Superoxide dismutases and superoxide reductases.Chemical reviews · 2014Review
- Neuron-specific expression of CuZnSOD prevents the loss of muscle mass and function that occurs in homozygous CuZnSOD-knockout mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Article
- Role of reactive oxygen species in the defective regeneration seen in aging muscle.Free radical biology & medicine · 2013Review
- Canine degenerative myelopathy: biochemical characterization of superoxide dismutase 1 in the first naturally occurring non-human amyotrophic lateral sclerosis model.Experimental neurology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of oxidative damage in neurodegenerative disease was investigated in mice lacking cytoplasmic Cu/Zn superoxide dismutase (SOD), created by deletion of the SOD1 gene (SOD1(-/-)). SOD1(-/-) mice developed a chronic peripheral hindlimb axonopathy. Mild denervation of muscle was detected at 2 months, and behavioral and physiological motor deficits were present at 5-7 months of age. Ventral root axons were shrunken but were normal in number. The somatosensory system in SOD1(-/-) mice was mildly affected. SOD1(-/-) mice expressing Cu/Zn SOD only in brain and spinal cord were generated using transgenic mice expressing mouse SOD1 driven by the neuron-specific synapsin promoter. Neuron-specific expression of Cu/Zn SOD in SOD1(-/-) mice rescued motor neurons from the neuropathy. Therefore, Cu/Zn SOD is not required for normal motor neuron survival, but is necessary for the maintenance of normal neuromuscular junctions by hindlimb motor neurons.
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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.