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通过METTL4-介导的线粒体DNA N6-甲基脱氧腺素促进巨细胞炎症和动脉样硬化

Longbin Zheng^1,2, Xiang Chen¹, Xian He¹

¹Key Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing, China (Longbin Zheng, X.C., X.H., Y.T., J.M., Xinyu Li, H.W., M.C., Y.Z., M.D., Q.Y., D.H., H.J., Xuesong Li, H.C.).

|December 17, 2024

概括

线粒体功能障碍导致动脉样硬化. 这项研究确定了METTL4 (甲基转移酶类蛋白4) 和其在线粒体DNA (mtDNA) 修饰中的作用作为一个关键因素,揭示了动脉样硬化的潜在治疗点.

科学领域:

分子生物学
表观遗传学
心血管研究

背景情况:

线粒体功能障碍是动脉形成的关键因素.
METTL4 (甲基转移酶类蛋白4) 通过N6-甲基脱氧腺素 (6mA) 来修改线粒体DNA (mtDNA).
在动脉样硬化中,METTL4介导的线粒基因调节的作用在很大程度上仍未被探索.

研究的目的:

研究METTL4在动脉样硬化中的作用.
为了阐明潜在的分子机制.
开发针对性治疗动脉样硬化的策略.

主要方法:

在动脉硬化病变中量化mtDNA6mA和METTL4水平.
使用Mettl4-Apoe淘汰和野生型小鼠,细胞模型和骨髓移植.
选METTL4抗剂的化合物库,并采用化向的嵌合体技术.

主要成果:

在斑块巨细胞中观察到mtDNA 6mA和METTL4表达的升高.
通过减少mtDNA6mA和恢复线粒体功能,Mettl4缺乏抑制了动脉样硬化进展.
抑制METTL4,特别是在pemetrexed和向药物合物时,可以缓解动脉样硬化.

结论:

在巨细胞线粒体功能障碍和动脉样硬化进展中,mtDNA 6mA和METTL4起着重要作用.
METTL4和mtDNA 6mA是动脉样硬化的有希望的治疗点.
向抑制METTL4,特别是在巨细胞中,提供了一个可行的治疗策略.

关键词:

在METTL4中动脉样硬化炎症的发生巨细胞线粒体

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