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与C1q/瘤坏死因子相关的蛋白-9增强巨细胞胆固醇排放,并通过AMPK激活改善逆胆固醇运输

Xiaosu Song¹, Gaizhen Liu¹, Yunfei Bin¹

¹Department of Cardiology, The Second Hospital of Shanxi Medical University, 382 Wuyi Road, Taiyuan, China.

Biochemical genetics

|April 10, 2024

概括

在小鼠中,C1q/瘤坏死因子相关蛋白-9 (CTRP9) 蛋白质的施用通过增强胆固醇外流和促进逆胆固醇运输 (RCT) 来降低动脉样硬化. 这种效应是由CTRP9激活AMPK信号传递的介导.

科学领域:

心血管生物学心血管生物学
代谢研究研究代谢研究
动脉样硬化病原体的产生

背景情况:

从泡细胞流出的胆固醇流出对于逆胆固醇运输 (RCT) 至关重要,这是一个关键的抗动脉产生过程.
ATP结合盒 (ABC) 载体ABCA1和ABCG1对于胆固醇排放至关重要.
一种阿迪波金的C1q/瘤亡因子相关蛋白-9 (CTRP9) 显示出动脉保护的潜力,但其在RCT中的作用尚不清楚.

研究的目的:

为了研究CTRP9对RCT和Atherosclerosis在ApoE淘汰赛小鼠的影响.
确定CTRP9在调节胆固醇外流和泡细胞中的ABC载体中的作用.

主要方法:

皮下注射CTRP9蛋白质给高脂肪饮食中的ApoE-/-小鼠.
对动脉样硬化病变的形成和肝脏ABCA1/ABCG1表达的评估.
使用RAW 264.7泡细胞进行体外研究,以评估CTRP9对胆固醇外流,ABC载体,LXR-α和AMPK信号传递的影响.

主要成果:

在ApoE-/-小鼠中,CTRP9治疗显著减少了动脉样硬化病变和增加胆固醇流量.
在CTRP9上调的肝脏ABCA1和ABCG1表达.
在体外,CTRP9剂量依赖地增加了ABCA1,ABCG1和LXR-α的表达,并激活了泡细胞中的AMPK信号.
通过AMP激活蛋白激酶 (AMPK) 敲击,取消了CTRP9-介导的胆固醇外流和输送器上调.

结论:

皮下CTRP9的使用是促进RCT和减少动脉样硬化的有效方法.
在动脉样硬化的动物模型中,CTRP9促进胆固醇外流,并促进RCT.
CTRP9的动脉动脉保护作用通过AMPK信号通路的激活来实现.

关键词:

这就是AMPKK.动脉样硬化是一种动脉样硬化.在CTRP9中使用.逆转胆固醇运输是指逆转胆固醇运输.

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