ArticleNeurospine2024
STM2457 Inhibits METTL3-Mediated m6A Modification of miR-30c to Alleviate Spinal Cord Injury by Inducing the ATG5-Mediated Autophagy.
Article in Neurospine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Emerging Regenerative Medicine for Spinal Cord Injury: Spinal Cord Organoids-on-a-Chip.International journal of molecular sciences · 2026Review
- Pharmacological METTL3 inhibition attenuates HIV-1 latency reversal in CD4Antimicrobial agents and chemotherapy · 2026Article
- Pharmacological METTL3 inhibition attenuates HIV-1 latency reversal in CD4bioRxiv : the preprint server for biology · 2026Article
- Article
- Extracellular Vesicle-Based Biomarkers in Spinal Cord Injury: A State-of-the-Art Review on Diagnostic and Prognostic Advances.International journal of molecular sciences · 2026Review
- Multimodal electroconductive PLGA-based scaffold orchestrates neuroprotection and regeneration following severe spinal cord injury.Journal of nanobiotechnology · 2026Article
- Injectable Poloxamer and Hyaluronic Acid Hydrogel for Sustained Co-Delivery of Dexamethasone and Lidocaine Ameliorates Neuropathic Pain.Biomaterials research · 2026Article
- Article
- Potential Pharmacologic Treatments in Spinal Cord Injury: A Narrative Review.Korean journal of neurotrauma · 2025Review
- Phenserine Mitigates Neuroinflammation, Apoptosis, and Behavioural Deficits to Enhance Motor Function and Recovery in a Mouse Model of Spinal Cord Injury.Molecular neurobiology · 2025Article
- Roles of METTL3 and NLRP3 in pyroptosis and prospects in SCIRI.Frontiers in immunology · 2025Review
- 3D bioprinted multifunctional GelMA/TMP scaffold integrated with neural stem cell-derived extracellular vesicles and neural progenitor cells for spinal cord injury repair.Journal of tissue engineeringArticle
- Comprehensive analysis of m6A RNA methylation regulators and the immune microenvironment in spinal cord injury.Frontiers in neurologyArticle
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Authors and funding
6 authors.
Funding
Abstract
objectiveThe study aimed to investigate the role of N6-methyladenosine (m6A) modification in spinal cord injury (SCI) and its underlying mechanism, focusing on the interplay between m6A methyltransferase-like 3 (METTL3), miR-30c, and autophagy-related proteins.
methodsAn SCI model was established in rats, and changes in autophagy-related proteins, m6A methylation levels, and miR-30c levels were analyzed. Hydrogen peroxide (H2O2)-stimulated spinal cord neuron cells (SCNCs) were used to assess the impact of METTL3 overexpression. The effects of STM2457, an antagonist of METTL3, were evaluated on cell viability, apoptosis, and autophagy markers in H2O2-stimulated SCNCs.
resultsIn the SCI model, decreased levels of autophagy markers and increased m6A methylation, miR-30c levels, and METTL3 were observed. Overexpression of METTL3 in SCNCs led to reduced cell viability, increased apoptosis, and suppressed autophagy. Conversely, co-overexpression of autophagy-related protein 5 (ATG5) or miR-30c inhibition reversed these effects. Knocking out METTL3 yielded opposite results. STM2457 treatment improved cell viability, reduced apoptosis, and upregulated autophagy markers in SCNCs, which also enhanced functional recovery in rats as measured by the Basso-Beattie-Bresnahan score and inclined plate test.
conclusionSTM2457 alleviated SCI by suppressing METTL3-mediated m6A modification of miR-30c, which in turn induces ATG5-mediated autophagy. This study provides insights into the role of m6A modification in SCI and suggests a potential therapeutic approach through targeting METTL3.
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