ArticleMolecular neurobiology2022
Identification of Ferroptotic Genes in Spinal Cord Injury at Different Time Points: Bioinformatics and Experimental Validation.
Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- TP53 drives neuronal ferroptosis by promoting KLHL4-mediated SLC7A11 ubiquitination after spinal cord injury.Neural regeneration research · 2026Article
- Blood-spinal cord barrier disruption after spinal cord injury: a time-dependent mechanistic review.Frontiers in cellular neuroscience · 2026Review
- Article
- PANoptosis: a new perspective for targeting programmed cell death after spinal cord injury.Frontiers in immunology · 2026Review
- Endoplasmic reticulum stress-mediated cell death in spinal cord injury: from molecular mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2026Review
- Machine Learning and Experiments Revealed Key Genes Related to PANoptosis Linked to Drug Prediction and Immune Landscape in Spinal Cord Injury.Molecular neurobiology · 2025Article
- The Interplay Between Endoplasmic Reticulum Stress and Ferroptosis in Neurological Diseases.Neurochemical research · 2025Review
- PGK1 Is Involved in the HIF-1 Signaling Pathway as a Hub Gene for Ferroptosis After Traumatic Brain Injury.Molecular neurobiology · 2025Article
- CHAC1: a master regulator of oxidative stress and ferroptosis in human diseases and cancers.Frontiers in cell and developmental biology · 2024Review
- Competing endogenous RNA network analysis of the molecular mechanisms of ischemic stroke.BMC genomics · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Programmed cell death (PCD) is an important pathologic process after spinal cord injury (SCI). As a new type of PCD, ferroptosis is involved in the secondary SCI. However, the underlying molecular mechanism remains unclear. In this study, we validated ferroptotic phenotype in an animal model of SCI. Then, the bioinformatic analyses performed on a microarray data of SCI (GSE45006). KEGG analysis suggested that the pathways of mTOR, HIF-1, VEGF, and protein process in endoplasmic reticulum were involved in SCI-induced ferroptosis. GO analysis revealed that oxidative stress, amide metabolic process, cation transport, and cytokine production were essential biological processes in ferroptosis after SCI. We highlighted five genes including ATF-3, XBP-1, HMOX-1, DDIT-3, and CHAC-1 as ferroptotic key gene in SCI. These results contribute to exploring the ferroptotic mechanism underlying the secondary SCI and providing potential targets for clinical treatment.
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Registered trials
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