ArticleMolecular neurobiology2021
Identification of Regeneration and Hub Genes and Pathways at Different Time Points after Spinal Cord Injury.
Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Regional Molecular Diversity in Chronic Spinal Cord Injury.Cellular and molecular neurobiology · 2026Article
- Pkd2l1 deletion inhibits the neurogenesis of cerebrospinal fluid-contacting neurons and impedes spinal cord injury repair.Cell death discovery · 2025Article
- CCL2 Knockdown Attenuates Inflammatory Response After Spinal Cord Injury Through the PI3K/Akt Signaling Pathway: Bioinformatics Analysis and Experimental Validation.Molecular neurobiology · 2024Article
- Annexin A1 in the nervous and ocular systems.Neural regeneration research · 2024Review
- Unbiased multitissue transcriptomic analysis reveals complex neuroendocrine regulatory networks mediated by spinal cord injury-induced immunodeficiency.Journal of neuroinflammation · 2023Article
- Identification of the CCL2 PI3K/Akt axis involved in autophagy and apoptosis after spinal cord injury.Metabolic brain disease · 2023Article
- Functions and mechanisms of cytosolic phospholipase ANeural regeneration research · 2023Review
- Identification of Ferroptotic Genes in Spinal Cord Injury at Different Time Points: Bioinformatics and Experimental Validation.Molecular neurobiology · 2022Article
- Identification of hub genes in the subacute spinal cord injury in rats.BMC neuroscience · 2022Article
- A Time-Course Study of the Expression Level of Synaptic Plasticity-Associated Genes in Un-Lesioned Spinal Cord and Brain Areas in a Rat Model of Spinal Cord Injury: A Bioinformatic Approach.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Spinal cord injury (SCI) is a neurological injury that can cause neuronal loss around the lesion site and leads to locomotive and sensory deficits. However, the underlying molecular mechanisms remain unclear. This study aimed to verify differential gene time-course expression in SCI and provide new insights for gene-level studies. We downloaded two rat expression profiles (GSE464 and GSE45006) from the Gene Expression Omnibus database, including 1 day, 3 days, 7 days, and 14 days post-SCI, along with thoracic spinal cord data for analysis. At each time point, gene integration was performed using "batch normalization." The raw data were standardized, and differentially expressed genes at the different time points versus the control were analyzed by Gene Ontology enrichment analysis, the Kyoto Encyclopedia of Genes and Genomes pathway analysis, and gene set enrichment analysis. A protein-protein interaction network was then built and visualized. In addition, ten hub genes were identified at each time point. Among them, Gnb5, Gng8, Agt, Gnai1, and Psap lack correlation studies in SCI and deserve further investigation. Finally, we screened and analyzed genes for tissue repair, reconstruction, and regeneration and found that Anxa1, Snap25, and Spp1 were closely related to repair and regeneration after SCI. In conclusion, hub genes, signaling pathways, and regeneration genes involved in secondary SCI were identified in our study. These results may be useful for understanding SCI-related biological processes and the development of targeted intervention strategies.
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