ArticleBioscience reports2023
miR-6315 silencing protects against spinal cord injury through the Smo and anti-ferroptosis pathway.
Article in Bioscience reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- MicroRNA-Ferroptosis-Spinal Cord Injury: A Complex Interplay in Neurodegeneration and Repair.International journal of molecular sciences · 2026Review
- Research progress on the Sonic Hedgehog signaling pathway in the central nervous system: Novel insights.Neural regeneration research · 2026Article
- miRNA-Mediated Regulation of Ferroptosis in Neurological Disorders: Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Ferroptosis in Spine-Related Diseases: Mechanistic Insights and Potential Therapeutic Targets.Cellular and molecular neurobiology · 2026Review
- Upregulation of miR-502-5p in traumatic spinal cord injury modulates neuroinflammation and oxidative stress by targeting FBXO28.Journal of orthopaedic surgery and research · 2025Article
- Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases.Signal transduction and targeted therapy · 2023Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) causes permanent damage and has a high disability rate. Currently, no efficient therapeutic strategy is available for SCI. The present study investigated the mechanisms of microRNAs (miRNAs) in rats with spinal cord injury. Whole transcriptome sequencing (WTS) was used for analyzing miRNA and messenger RNA (mRNA) expression patterns in rat spinal cord tissue at different time points after SCI. Gene Ontology (GO) and KEGG pathways were analyzed to obtain crucial functional pathways. miR-6315 was the most significantly up-regulated and differentially expressed miRNA after 24 h of SCI; the expression of miR-6315 gradually decreased after 3 and 7 days of SCI. Bioinformatics analysis was conducted to predict the targeting relation of miR-6315 with Smo, and qRT-PCR and dual-luciferase reporter assays were conducted for verification. The miR-6315 silencing (miR-6315-si) adenovirus was successfully constructed. miR-6315 knockdown treatment significantly promoted functional behavioral recovery in rats post-SCI through using Basso-Beattie-Bresnahan (BBB) locomotor rating scale and the inclined plane test. The neuronal axon regeneration and neuronal migration were promoted, and cell apoptosis was attenuated in treated SCI rats and Glu-treated neurons after miR-6315 knockdown using immunofluorescence and scratch assays. We discovered that Smo and anti-ferroptosis pathway factors, xCT, GSH, and GPX4, may be involved in miR-6315-regulated SCI repair. The expression of miR-6315 was negatively correlated with Smo, xCT, GSH, and GPX4. In conclusion, miR-6315 may be a potential target in the treatment of SCI.
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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.