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UQCRB通过在动脉样硬化内皮功能障碍中促进COX5 A来调节线粒体能量代谢

Rui Dai¹, Xiaotong Lei², Xiaojun Liu¹

¹Department of Cardiology, Xuzhou First People's Hospital (The Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University), Xuzhou, China.

Naunyn-Schmiedeberg's archives of pharmacology

|May 30, 2025

概括

乌比基诺-细胞染色体c还原酶结合蛋白 (UQCRB) 通过上调COX5A,改善线粒体功能和减少炎症来预防动脉样硬化. 准UQCRB为动脉样硬化治疗提供了一个新的治疗策略.

科学领域:

心血管生物学心血管生物学
线粒体医学线粒体医学
分子生物学分子生物学

背景情况:

线粒体功能障碍是动脉样硬化 (AS) 病变的核心.
乌比基诺-细胞染色体c减酶结合蛋白 (UQCRB) 是线粒体呼吸链的关键组成部分.
在AS相关的内皮功能障碍中UQCRB的作用需要阐明.

研究的目的:

调查UQCRB对AS内皮功能障碍的保护作用.
为了确定UQCRB是否可调节细胞染色体c氧化酶子单元5A (COX5A).
评估UQCRB对线粒体能量代谢,炎症和AS中的亡的影响.

主要方法:

生物信息学分析和临床数据,以评估AS中的UQCRB水平.
在体外实验中,UQCRB过度表达对氧化低密度脂蛋白 (OX-LDL) 的反应.
在体内研究中,使用AS小鼠模型治疗UQCRB向化合物特尔佩斯塔.

主要成果:

在AS患者中,UQCRB的下调;UQCRB过度表达增强了线粒体功能 (膜潜力,ATP生产),减少了ROS,炎症 (TNF-α,IL-1β,IL-6),亡和粘附分子 (ICAM-1,VCAM-1) 在体外.
观察到AMPK通路的UQCRB激活.
在AS小鼠模型中,准UQCRB的特尔佩斯塔辛使内皮功能障碍恶化和炎症增加.

结论:

UQCRB上调COX5A,从而增强线粒体能量代谢,并激活AMPK通路.
在AS中,UQCRB有效降低了炎症和亡.
UQCRB代表了预防和治疗动脉样硬化的有前途的治疗标.

关键词:

动脉样硬化是一种动脉样硬化.这就是COX5A.内皮质功能障碍内皮质功能障碍炎症炎症是一种炎症.在UQCRB中,UQCRB是最重要的.

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