m6A甲基化修饰在急性肾损伤中的研究进展

Research progress on the relationship between m6A methylation modification and acute kidney injury

急性肾损伤因高发病率、高病死率、高治疗费用已然成为全球性重要公共健康问题,其发病机制复杂、治疗策略有限,深入探索其病理生理机制、寻找临床治疗的潜在靶点具有重要意义。N6-甲基腺嘌呤(m6A)甲基化是真核生物中最为普遍和高度保守的表观遗传修饰,是由m6A甲基转移酶、去甲基化酶和阅读蛋白共同调控RNA的剪接、出核、翻译、稳定性和高级结构的动态可逆过程。研究表明m6A甲基化修饰在急性肾损伤的发生发展中发挥重要调节作用,有望成为治疗急性肾损伤的有效靶点。本文就m6A在急性肾损伤中的调控作用及未来可能的研究方向进行综述。

Acute kidney injury(AKI)is a global public health problem with high morbidity,high mortality and costly treatment cost.The pathogenesis of AKI is very complex,and the treatment strategies for AKI are lim⁃ited,then it is very matter to explore the pathophysiological mechanism and potential therapeutic targets of acute kidney injury.N6-methyladenosine(m6A)is the most abundant and extremely conservative epigenetic modification in eukaryotic,which is a dynamic and reversible process involving in splicing,nuclear export,translation,stabil⁃ity,and higher structure of RNA,and regulated by three regulatory factors:methyltransferase,demethylase and methylated reading protein.Current studies have found that m6A plays an important regulatory role in AKI and can be a potential therapeutic target for AKI.In this review,we provide a brief description of m6A and summarize the impact of m6A on AKI and possible future study directions for this research.