脂肪量和肥胖相关蛋白介导的N^(6)-腺苷酸甲基化在动脉粥样硬化中的研究进展  

Advances in fat mass and obesity-related protein-mediated N^(6)-adenylate methylation in atherosclerosis

作　　者：谢卓熠 陈宋涛 孙璇 羊佩娟 陈雅丽 桂庆军 左建宏 XIE Zhuoyi;CHEN Songtao;SUN Xuan;YANG Peijuan;CHEN Yali;GUI Qinjun;ZUO Jianhong(Institute of Translational Medicine,Hengyang Medical College,University of South China,Hengyang,Hunan 421001,China;Guangxi Key Laboratory of Diabetic Systems Medicine,Guilin Medical University,Guilin,Guangxi 541106,China)

机构地区：[1]南华大学衡阳医学院转化医学研究所,湖南省衡阳市421001 [2]桂林医学院广西糖尿病系统医学重点实验室,广西桂林市541106

出　　处：《中国动脉硬化杂志》2025年第3期257-263,共7页Chinese Journal of Arteriosclerosis

基　　金：湖南省自然科学基金项目(2022JJ30515);湖南省大学生创新训练计划项目(S202310555220)。

摘　　要：N^(6)-腺苷酸甲基化是真核生物中最普遍的mRNA修饰,脂肪量和肥胖相关蛋白是其去甲基化酶,可有效去除mRNA的N^(6)-腺苷酸甲基化修饰,与肥胖密切相关。动脉粥样硬化是一种脂质驱动的血管壁慢性炎症性病变。研究发现脂肪量和肥胖相关蛋白介导的N^(6)-腺苷酸甲基化可能通过脂代谢、氧化应激、线粒体功能障碍以及巨噬细胞泡沫化影响动脉粥样硬化的进程。N^(6)-methyladenosine(m 6A)is the most common mRNA modification in eukaryotes,and fat mass and o besity-related protein(FTO),are its demethylases,which efficiently remove the modification of m 6A mRNA,and is strongly associated with obesity.Atherosclerosis is a chronic inflammatory lesion of the blood vessel wall driven by lipids.It was found that FTO-mediated m 6A may influence the process of atherosclerosis through lipid metabolism,oxidative stress,mitochondrial dysfunction,and macrophage foaminess.

关 键 词：脂肪量和肥胖相关蛋白 N^(6)-腺苷酸甲基化 动脉粥样硬化 

分 类 号：R365[医药卫生—病理学] R5[医药卫生—基础医学]