ArticleNeural regeneration research2026
Integrating bulk and single-cell transcriptome profiling to uncover diagnostic biomarkers and regulatory mechanisms of oxidative stress in spinal cord injury.
Article in Neural regeneration research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Mitochondrial-Inflammatory Axis Dysregulation Triggers Disulfidptosis and the Multifaceted Protective Mechanism of Bisphenol A Following Spinal Cord Injury.Molecular neurobiology · 2026Article
- Investigating the efficacy, methods, and challenges of induced pluripotent stem cells (iPSC) therapy in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
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12 authors.
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Abstract
JOURNAL/nrgr/04.03/01300535-202606000-00079/figure1/v/2026-02-11T151048Z/r/image-tiff Oxidative stress significantly contributes to secondary damage after spinal cord injury. Despite its importance, research on oxidative stress in spinal cord injury remains limited. Investigating the expression and regulation of oxidative stress-related genes could enhance the diagnosis and treatment of spinal cord injury. In this study, we analyzed the sequencing data of human blood samples and injured mouse spinal cord tissue that were sourced from GEO databases and identified diagnostic biomarkers associated with the severity of spinal cord injury. We also explored the expression patterns of oxidative stress-related genes, potential regulatory mechanisms, and therapeutic drugs. To validate our findings, we performed immunofluorescence and quantitative polymerase chain reaction to assess gene expression in the injured spinal cord. Our results revealed biomarkers associated with oxidative stress and immune responses across different levels of spinal cord injury in humans. We identified differentially expressed oxidative stress-related genes and key hub genes in injured mouse spinal cord tissue and revealed their temporal expression patterns at both the tissue and single-cell levels. We also clarified the signaling pathways associated with oxidative stress and identified ligand-receptor pairs among various cell types at different time points after injury. Furthermore, we discovered microRNAs, long non-coding RNAs, and transcription factors that regulate these hub genes and revealed their roles in modulating gene expression at various stages after spinal cord injury. We also identified drugs targeting these hub genes. The findings from this study not only aid in identifying diagnostic biomarkers that reflect the severity of spinal cord injury, but also provide insights into the expression dynamics of oxidative stress-related genes. In addition, the study reveals potential regulatory mechanisms and identifies potential drugs to treat patients with spinal cord injury.
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