In addition to DNA methylation, reversible epigenetic modification occurring in RNA has been discovered recently. The most abundant type of RNA methylation is N6-methyladenosine (m6A) modification, which is dynamically regulated by methylases (“writers”), demethylases (“erasers”) and m6A-binding proteins (“readers”). As an essential posttranscriptional regulator, m6A can control mRNA splicing, processing, stability, export and translation. Recent studies have revealed that m6A modification has the strongest tissue specificity for brain tissue and plays crucial roles in central nervous system (CNS) injures by affecting its downstream target genes or non-coding RNAs. This review focuses on the expression and function of m6A regulatory proteins in CNS trauma in vitro and in vivo. We also highlight the latest insights into the molecular mechanisms of pathological damage in the CNS. Understanding m6A dynamics, functions, and machinery will yield an opportunity for designing and developing novel therapeutic agents for CNS injuries.

除了 DNA 甲基化之外，最近还发现了发生在 RNA 中的可逆表观遗传修饰。最丰富的 RNA 甲基化类型是 N6-甲基腺苷 (m6A) 修饰，它由甲基化酶（“写入器”）、去甲基化酶（“擦除器”）和 m6A 结合蛋白（“读取器”）动态调节。作为必不可少的转录后调节因子，m6A 可以控制 mRNA 的剪接、加工、稳定性、输出和翻译。最近的研究表明，m6A 修饰对脑组织具有最强的组织特异性，并通过影响其下游靶基因或非编码 RNA 在中枢神经系统 (CNS) 损伤中发挥关键作用。本综述的重点是 m6A 调节蛋白在体外和体内中枢神经系统创伤中的表达和功能. 我们还强调了对中枢神经系统病理损伤分子机制的最新见解。了解 m6A 动力学、功能和机制将为设计和开发用于 CNS 损伤的新型治疗剂提供机会。