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删除METTL14,一个关键的甲基化调节剂,减轻了血管衰老

Xin Liu^1,2,3, Heng Liu^1,2,3, Yuan Lin^1,2,3

¹State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Department of Pharmacology, College of Pharmacy, and Department of Cardiology, The Second Affiliated Hospital, Harbin Medical University, 157 Baojian Road, Harbin 150081, China.

European heart journal

|August 4, 2025

概括

甲基转移酶样蛋白14 (METTL14) 通过通过METTL14/Toll样受体4 (TLR4) 途径促进炎症,驱动血管衰老. 抑制METTL14可以治疗血管衰老和相关疾病.

科学领域:

分子生物学分子生物学
血管生物学血管生物学
衰老研究研究衰老研究

背景情况:

血管衰老与炎症有关,导致血管疾病.
慢性血管炎症和病理变化的关键触发因素仍未得到充分研究.
甲基转移酶样蛋白14 (METTL14) 正在研究其在衰老期间血管炎症中的作用.

研究的目的:

为了研究METTL14在血管衰老的发病过程中的炎症中的作用.
阐明将METTL14与血管衰老联系起来的分子机制.

主要方法:

利用自然和D-银河糖诱导衰老的小鼠模型.
产生的内皮细胞特异性METTL14淘汰小鼠.
研究了METTL14在人类和小鼠内皮细胞,包括衰老细胞中的作用.

主要成果:

在老年人和老鼠大动脉内皮细胞和老化的内皮细胞中,METTL14被上调.
METTL14敲除/敲除改善了血管衰老表型 (动脉硬,重塑,衰老) 和细胞衰老,炎症和氧化应激.
METTL14增强了托尔类受体4 (TLR4) 的mRNA稳定性,TLR4的淘汰扭转了METTL14的有害影响;METTL14和TLR4的升高与人类的血管衰老相关.

结论:

METTL14/TLR4信号通路在血管衰老的发病过程中起着至关重要的作用.
降低METTL14是一种潜在的治疗策略,可以缓解血管衰老和诸如动脉样硬化和动脉样硬化等相关疾病.

关键词:

动脉的硬性动脉的硬性内皮细胞是内皮细胞.炎症炎症是一种炎症.甲基转移酶类蛋白14 类似的蛋白质收费类受体4 收费类受体4 血管衰老血管衰老

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