ArticleHeliyon2024
LncRNA OIP5-AS1 regulates ferroptosis and mitochondrial dysfunction-mediated apoptosis in spinal cord injury by targeting the miR-128-3p/Nrf2 axis.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- MicroRNA-Ferroptosis-Spinal Cord Injury: A Complex Interplay in Neurodegeneration and Repair.International journal of molecular sciences · 2026Review
- mRedox biology · 2026Review
- miRNA-Mediated Regulation of Ferroptosis in Neurological Disorders: Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Expression and Clinical Significance of the Long Non-Coding RNA OIP5-AS1 in Alcohol Use Disorder.Addiction biology · 2026Article
- Ferroptosis-associated transcriptional factors in neurological diseases: molecular mechanisms and therapeutic prospects.Experimental & molecular medicine · 2025Review
- KDM6B promotes ferroptosis in rheumatoid arthritis fibroblast-like synoviocytes via the miR-128-3p/SLC7A11 axis through H3K27me3 modification.Journal of orthopaedic surgery and research · 2025Article
- NcRNAs: a potential treatment for spinal cord injury.Frontiers in cellular neuroscience · 2025Review
- Mechanistic insights into Nrf2-driven pathogenesis and therapeutic targeting in spinal cord injury.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ferroptosis is an important way of neuronal cell death in acute phase and participates in the inflammatory cascade after spinal cord injury (SCI). It is reported that microRNA (miRNA) and long non-coding RNA (lncRNA) are key mediators in the regulation of ferroptosis. This study will explore the inhibitory effect of LncRNA OIP5-AS1 on ferroptosis and mitochondrial dysfunction-mediated apoptosis in SCI. Methods: The ferric ammonium citrate (FAC)-induced cell model and the SCI rat model were established. The expression of LncRNA OIP5-AS1, miR-128-3p and Nrf2 were transfected to evaluated the effect on the viability and apoptosis of FAC-induced cell. The interaction between LncRNA OIP5-AS1 and miR-128-3p or miR-128-3p and Nrf2 were analyzed. In addition, expressions of markers related to ferroptosis and mitochondrial dysfunction were analyzed in vitro and in vivo. Histopathologic slide staining was used to analyze spinal cord injury in vivo. Results: LncRNA OIP5-AS1 expression was abnormally down-regulated in FAC-induced SCI cell model and SCI rats. The LncRNA OIP5-AS1 deficiency induced decreased Nrf2 level by less sponging miR-128-3p, thus, aggravating spinal cord injury and inducing more apoptosis, ferroptosis and mitochondrial dysfunction in neural stem cells with SCI. However, overexpression of LncRNA OIP5-AS1 inhibited apoptosis, ferroptosis and mitochondrial dysfunction, thus effectively ameliorating spinal cord injury. Conclusion: This finding demonstrates that LncRNA OIP5-AS1 overexpression could enhance the recovery of spinal cord injury by regulating the miR-128-3p/Nrf2 axis.
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