ArticleCell death discovery2022
METTL14 promotes apoptosis of spinal cord neurons by inducing EEF1A2 m6A methylation in spinal cord injury.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The trial behind it
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Interaction between N6-methyladenosine (mGenes & diseases · 2026Review
- The identification of genes related to METTL14 inhibition in radiation-induced hepatocyte death based on bioinformatics analysis.Scientific reports · 2026Article
- Spinal motor neuron degeneration after brachial plexus avulsion: mechanisms and therapeutic targets.Frontiers in neuroscience · 2026Review
- New Diagnostic and Therapeutic Targets for Spinal Cord Injury: GRN Gene.Journal of cellular and molecular medicine · 2025Article
- GPR30 Inhibits Neuronal Apoptosis After Subarachnoid Hemorrhage by Activating the Wnt/β-Catenin Pathway in a m6A-dependent Manner.Molecular neurobiology · 2025Article
- The Role of Methylation Modification in Neural Injury and Repair.International journal of molecular sciences · 2025Review
- Long non-coding RNA GAS5 promotes neuronal apoptosis in spinal cord injuryWorld journal of orthopedics · 2025Article
- IGF2BP2 Regulates the Progression of Alzheimer's Disease Through m6A-Mediated NLRP3 Inflammasome.Immunity, inflammation and disease · 2025Article
- Characterization of the Expressions and m6A Methylation Modification Patterns of mRNAs and lncRNAs in a Spinal Cord Injury Rat Model.Molecular neurobiology · 2025Article
- METTL14 regulates inflammation in ulcerative colitis via the lncRNA DHRS4-AS1/miR-206/A3AR axis.Cell biology and toxicology · 2024Article
- Mechanism of Mettl14 regulating AIM2 inflammasome activation and neuronal apoptosis and pyroptosis in spinal cord injury by mediating PPARγ m6A methylation.Journal of physiology and biochemistry · 2024Article
- Exploiting Translation Machinery for Cancer Therapy: Translation Factors as Promising Targets.International journal of molecular sciences · 2024Review
- Sevoflurane augments neuroinflammation by regulating DUSP6 via YTHDF1 in postoperative cognitive dysfunction.Toxicology research · 2024Article
- Resveratrol Enhances Antioxidant and Anti-Apoptotic Capacities in Chicken Primordial Germ Cells through m6A Methylation: A Preliminary Investigation.Animals : an open access journal from MDPI · 2024Article
- A neural mScience China. Life sciences · 2024Article
- METTL3 promotes microglial inflammation via MEF2C in spinal cord injury.Cell and tissue research · 2024Article
- METTL14 Regulates the m6A Modification of TRAF6 to Suppress Mitochondrial Dysfunction and Ferroptosis in Dopaminergic Neurons via the cGAS-STING Pathway.Current molecular medicine · 2024Article
- Upregulation of UBR1 m6A Methylation by METTL14 Inhibits Autophagy in Spinal Cord Injury.eNeuro · 2023Article
- METTL3 Affects Spinal Cord Neuronal Apoptosis by Regulating Bcl-2 m6A Modifications After Spinal Cord Injury.Neurospine · 2023Article
- Identification of the CCL2 PI3K/Akt axis involved in autophagy and apoptosis after spinal cord injury.Metabolic brain disease · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) is a devastating traumatic condition. METTL14-mediated m6A modification is associated with SCI. This study was intended to investigate the functional mechanism of RNA methyltransferase METTL14 in spinal cord neuron apoptosis during SCI. The SCI rat model was established, followed by evaluation of pathological conditions, apoptosis, and viability of spinal cord neurons. The neuronal function of primary cultured spinal motoneurons of rats was assessed after hypoxia/reoxygenation treatment. Expressions of EEF1A2, Akt/mTOR pathway-related proteins, inflammatory cytokines, and apoptosis-related proteins were detected. EEF1A2 was weakly expressed and Akt/mTOR pathway was inhibited in SCI rat models. Hypoxia/Reoxygenation decreased the viability of spinal cord neurons, promoted LDH release and neuronal apoptosis. EEF1A2 overexpression promoted the viability of spinal cord neurons, inhibited neuronal apoptosis, and decreased inflammatory cytokine levels. Silencing METTL14 inhibited m6A modification of EEF1A2 and increased EEF1A2 expression while METTL14 overexpression showed reverse results. EEF1A2 overexpression promoted viability and inhibited apoptosis of spinal cord neurons and inflammation by activating the Akt/mTOR pathway. In conclusion, silencing METTL14 repressed apoptosis of spinal cord neurons and attenuated SCI by inhibiting m6A modification of EEF1A2 and activating the Akt/mTOR pathway.
Identifiers
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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.