ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Neuron-specific expression of CuZnSOD prevents the loss of muscle mass and function that occurs in homozygous CuZnSOD-knockout mice.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 90 citations in OpenAlex.
- Episodic denervation as a driver of loss of skeletal muscle redox homeostasis and muscle weakness in sarcopenia: Possible amelioration by exercise.Sports medicine and health science · 2025Review
- Skeletal muscle innervation: Reactive oxygen species as regulators of neuromuscular junction dynamics and motor unit remodeling.Free radical biology & medicine · 2025Review
- Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025Review
- Potential relationship between cuproptosis and sepsis-acquired weakness: an intermediate role for mitochondria.Frontiers in physiology · 2025Review
- Mouse models used to test the role of reactive oxygen species in aging and age-related chronic diseases.Free radical biology & medicine · 2024Review
- Neuroprotective treatment with the nitrone compound OKN-007 mitigates age-related muscle weakness in aging mice.GeroScience · 2024Article
- Associations between blood manganese levels and sarcopenia in adults: insights from the National Health and Nutrition Examination Survey.Frontiers in public health · 2024Article
- Intermittent treatment with elamipretide preserves exercise tolerance in aged female mice.GeroScience · 2023Article
- Deletion ofeNeuro · 2023Article
- Acylated Ghrelin Receptor Agonist HM01 Decreases Lean Body and Muscle Mass, but Unacylated Ghrelin Protects against Redox-Dependent Sarcopenia.Antioxidants (Basel, Switzerland) · 2022Article
- Impact of aging and oxidative stress on specific components of excitation contraction coupling in regulating force generation.Science advances · 2022Article
- Skeletal muscle transcriptomics identifies common pathways in nerve crush injury and ageing.Skeletal muscle · 2022Article
- Muscle mitochondrial catalase expression prevents neuromuscular junction disruption, atrophy, and weakness in a mouse model of accelerated sarcopenia.Journal of cachexia, sarcopenia and muscle · 2021Article
- Deletion of Neuronal CuZnSOD Accelerates Age-Associated Muscle Mitochondria and Calcium Handling Dysfunction That Is Independent of Denervation and Precedes Sarcopenia.International journal of molecular sciences · 2021Article
- Redox Signaling and Sarcopenia: Searching for the Primary Suspect.International journal of molecular sciences · 2021Review
- Murine muscle stem cell response to perturbations of the neuromuscular junction are attenuated with aging.eLife · 2021Article
- Transgenic expression of SOD1 specifically in neurons of Sod1 deficient mice prevents defects in muscle mitochondrial function and calcium handling.Free radical biology & medicine · 2021Article
- Review
- On the mechanisms underlying attenuated redox responses to exercise in older individuals: A hypothesis.Free radical biology & medicine · 2020Article
- Neuron-specific deletion of CuZnSOD leads to an advanced sarcopenic phenotype in older mice.Aging cell · 2020Article
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
Deletion of copper-zinc superoxide dismutase (CuZnSOD) in Sod1(-/-) mice leads to accelerated loss of muscle mass and force during aging, but the losses do not occur with muscle-specific deletion of CuZnSOD. To determine the role of motor neurons in the muscle decline, we generated transgenic Sod1(-/-) mice in which CuZnSOD was expressed under control of the synapsin 1 promoter (SynTgSod1(-/-) mice). SynTgSod1(-/-) mice expressed CuZnSOD in brain, spinal cord, and peripheral nerve, but not in other tissues. Sciatic nerve CuZnSOD content in SynTgSod1(-/-) mice was ~20% that of control mice, but no reduction in muscle mass or isometric force was observed in SynTgSod1(-/-) mice compared with control animals, whereas muscles of age-matched Sod1(-/-) mice displayed 30-40% reductions in mass and force. In addition, increased oxidative damage and adaptations in stress responses observed in muscles of Sod1(-/-) mice were absent in SynTgSod1(-/-) mice, and degeneration of neuromuscular junction (NMJ) structure and function occurred in Sod1(-/-) mice but not in SynTgSod1(-/-) mice. Our data demonstrate that specific CuZnSOD expression in neurons is sufficient to preserve NMJ and skeletal muscle structure and function in Sod1(-/-) mice and suggest that redox homeostasis in motor neurons plays a key role in initiating sarcopenia during aging.
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