心肌梗死（MI）严重威胁人类健康。研究表明长链非编码RNA（LncRNA）与MI的发生关系密切，但具体机制尚未完全清楚。N6-甲基腺嘌呤（m6A）修饰是LncRNA发挥调控功能的重要机制，我们前期研究发现MI时LncRNA XIST和调控m6A甲基化修饰的RBM15/15B表达均上调。此外有研究表明LncRNA XIST可调控炎症反应且与RNF20有关。据此我们提出假说：RBM15/15B调控MI中LncRNA XIST m6A甲基化，而LncRNA XIST m6A甲基化后通过RNF20/NF-κB轴激活MI炎症反应，加重心肌损伤。本项目拟从分子、细胞和整体水平，通过建立心肌细胞、在体MI模型，利用siRNA、基因敲除、薄层色谱法、RNA免疫共沉淀、RNA pull-down等方法，深入研究MI中m6A修饰调控LncRNA XIST激活炎症的作用机制，为MI治疗提供一种新的思路

Myocardial infarction (MI) is a serious threat to human health. Long non-coding RNA (LncRNA) is closely related to MI, but little is known about its mechanism of action. N6-methyladenine (m6A) modification is an important regulatory mechanism of LncRNA. We found that the expression of LncRNA XIST and RBM15/15B were up-regulated in MI. In addition, studies have shown that LncRNA XIST can regulate inflammation and is related to RNF20. The hypothesis is that RBM15/15B regulates the methylation of LncRNA XIST in MI, while LncRNA XIST methylation aggravates myocardial injury by activating the inflammation through RNF20/NF-kappa B axis in MI . The aim of this project is to establish myocardial cells and in vivo MI models. The functions and mechanisms of LncRNA in MI are discussed by using siRNA, gene knockout, TLC, RNA immunoprecipitation, pull-down and qPCR. This study will reveal the mechanism of MI from the new perspective of LncRNA m6A methylation activating inflammation, and provide a new idea for the treatment of MI.