ReviewFrontiers in cellular neuroscience2022
N6-methyladenosine modification: A potential regulatory mechanism in spinal cord injury.
Review in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- METTL3 promotes proliferation and invasion and inhibits ferroptosis in hepatocellular carcinoma by mediating m6A methylation modification of NUPR1.Molecular and cellular biochemistry · 2026Article
- Transcriptomics Insights into Spinal Cord Injury for Therapy Development.International journal of molecular sciences · 2026Review
- New Diagnostic and Therapeutic Targets for Spinal Cord Injury: GRN Gene.Journal of cellular and molecular medicine · 2025Article
- The Role of Methylation Modification in Neural Injury and Repair.International journal of molecular sciences · 2025Review
- m6A-related genes of peripheral white blood cell in spinal cord injury as potential targets for prognosis and treatment.Frontiers in medicine · 2025Article
- Mechanism of Fat Mass and Obesity-Related Gene-Mediated Heme Oxygenase-1 m6A Modification in the Recovery of Neurological Function in Mice with Spinal Cord Injury.Orthopaedic surgery · 2024Article
- Inhibition of UTX/KDM6A improves recovery of spinal cord injury by attenuating BSCB permeability and macrophage infiltration through the MLCK/p-MLC pathway.Journal of neuroinflammation · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A), an essential post-transcriptional modification in eukaryotes, is closely related to the development of pathological processes in neurological diseases. Notably, spinal cord injury (SCI) is a serious traumatic disease of the central nervous system, with a complex pathological mechanism which is still not completely understood. Recent studies have found that m6A modification levels are changed after SCI, and m6A-related regulators are involved in the changes of the local spinal cord microenvironment after injury. However, research on the role of m6A modification in SCI is still in the early stages. This review discusses the latest progress in the dynamic regulation of m6A modification, including methyltransferases ("writers"), demethylases ("erasers") and m6A -binding proteins ("readers"). And then analyses the pathological mechanism relationship between m6A and the microenvironment after SCI. The biological processes involved included cell death, axon regeneration, and scar formation, which provides new insight for future research on the role of m6A modification in SCI and the clinical transformation of strategies for promoting recovery of spinal cord function.
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Registered trials
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