ArticleBrain : a journal of neurology2015
Neuron-specific antioxidant OXR1 extends survival of a mouse model of amyotrophic lateral sclerosis.
Article in Brain : a journal of neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 87 citations in OpenAlex.
- TLDc proteins: Stress-responsive nexus regulators of redox signaling, V-ATPase dynamics, and organellar crosstalk in neurodegeneration.Redox biology · 2026Review
- Integrated multi-omics identification of m6A-SNP-related diagnostic biomarkers in amyotrophic lateral sclerosis.Frontiers in immunology · 2026Article
- Transcriptomic profiles of susceptibility and resilience to stress in the amygdala and hippocampus of male rats.Neurobiology of stress · 2025Article
- Single-Cell Transcriptomic Profiling Reveals Regional Differences in the Prefrontal and Entorhinal Cortex of Alzheimer's Disease Brain.International journal of molecular sciences · 2025Article
- Oxidative Stress in Brain Function.Antioxidants (Basel, Switzerland) · 2025Review
- Exercise, disease state and sex influence the beneficial effects of Fn14-depletion on survival and muscle pathology in the SOD1Skeletal muscle · 2024Article
- Review
- Neuroinflammation and Lysosomal Abnormalities Characterise the Essential Role for Oxidation Resistance 1 in the Developing and Adult Cerebellum.Antioxidants (Basel, Switzerland) · 2024Article
- OXR1 maintains the retromer to delay brain aging under dietary restriction.Nature communications · 2024Article
- TLDc Domain-Containing Genes in Autism Spectrum Disorder: New Players in the Oxidative Stress Response.International journal of molecular sciences · 2023Article
- A loss-of-function mutation in human Oxidation Resistance 1 disrupts the spatial-temporal regulation of histone arginine methylation in neurodevelopment.Genome biology · 2023Article
- The landscape of cognitive impairment in superoxide dismutase 1-amyotrophic lateral sclerosis.Neural regeneration research · 2023Review
- Stem Cells From Human Exfoliated Deciduous Teeth-Conditioned Medium (SHED-CM) is a Promising Treatment for Amyotrophic Lateral Sclerosis.Frontiers in pharmacology · 2022Article
- Delivery of pOXR1 through an injectable liposomal nanoparticle enhances spinal cord injury regeneration by alleviating oxidative stress.Bioactive materials · 2021Article
- Oxidative Stress Resistance 1 Gene Therapy Retards Neurodegeneration in the rd1 Mutant Mouse Model of Retinopathy.Investigative ophthalmology & visual science · 2021Article
- Locomotor deficits in a mouse model of ALS are paralleled by loss of V1-interneuron connections onto fast motor neurons.Nature communications · 2021Article
- Why Do Muse Stem Cells Present an Enduring Stress Capacity? Hints from a Comparative Proteome Analysis.International journal of molecular sciences · 2021Article
- A Novel Supplement Attenuates Oxidative Stress-Induced TDP-43-Related Pathogenesis in TDP-43-Expressed Cells.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- OXR2 Increases Plant Defense against a Hemibiotrophic Pathogen via the Salicylic Acid Pathway.Plant physiology · 2020Article
- ZebrafishGenes · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis is a devastating neurodegenerative disorder characterized by the progressive loss of spinal motor neurons. While the aetiological mechanisms underlying the disease remain poorly understood, oxidative stress is a central component of amyotrophic lateral sclerosis and contributes to motor neuron injury. Recently, oxidation resistance 1 (OXR1) has emerged as a critical regulator of neuronal survival in response to oxidative stress, and is upregulated in the spinal cord of patients with amyotrophic lateral sclerosis. Here, we tested the hypothesis that OXR1 is a key neuroprotective factor during amyotrophic lateral sclerosis pathogenesis by crossing a new transgenic mouse line that overexpresses OXR1 in neurons with the SOD1(G93A) mouse model of amyotrophic lateral sclerosis. Interestingly, we report that overexpression of OXR1 significantly extends survival, improves motor deficits, and delays pathology in the spinal cord and in muscles of SOD1(G93A) mice. Furthermore, we find that overexpression of OXR1 in neurons significantly delays non-cell-autonomous neuroinflammatory response, classic complement system activation, and STAT3 activation through transcriptomic analysis of spinal cords of SOD1(G93A) mice. Taken together, these data identify OXR1 as the first neuron-specific antioxidant modulator of pathogenesis and disease progression in SOD1-mediated amyotrophic lateral sclerosis, and suggest that OXR1 may serve as a novel target for future therapeutic strategies.
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