ArticleBMC genomics2025
Genome-wide analysis of lncRNA m6A methylation in the mouse cortex after repetitive mild traumatic brain injury.
Article in BMC genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
9 authors.
Funding
Abstract
N6-methyladenosine (m6A), a prevalent post-transcriptional modification in eukaryotic RNA, plays a significant role in regulating sensory experiences, learning, and injury in the mammalian central nervous system. However, the pattern of lncRNA m6A methylation in the mouse cortex following repetitive mild traumatic brain injury (rmTBI) has not been explored. This study conducted a genome-wide analysis of lncRNA m6A methylation in the mouse cortex using methylated RNA immunoprecipitation sequencing (MeRIP-Seq). We identified 43,103 differentially methylated peaks. Notably, the expression of m6A peaks indicated altered methylation and expression levels of 423 lncRNAs after rmTBI. In addition, employing METTL3 inhibitor STM2457 demonstrated that functional METTL3 was essential for repairing neural damage caused by rmTBI and influenced spatial learning and memory in rmTBI-model mice. Thus, the m6A methylation pattern of lncRNA in the mouse cortex after rmTBI identifies METTL3 as a potential intervention target for epigenetic modification following such injuries. Clinical trial number Not applicable.
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