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同类半氨酸调节CXCL10/CXCR3轴活动,诱导内皮功能障碍

Yanjie Xu¹, Yingying Xu², Zuozong Yu³

¹Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China. xuyanjie13@163.com.

Cellular and molecular biology (Noisy-le-Grand, France)

|March 2, 2024

概括

高水平的homocysteine (Hcy) 损害了血管内膜,导致内皮功能障碍. 准CXCL10/CXCR3通路可以防止这些有害影响和心血管疾病.

科学领域:

心血管生物学心血管生物学
内皮细胞生物学内皮细胞生物学
分子医学是分子医学.

背景情况:

高水平的同类氨酸 (Hcy) 是心血管疾病的危险因素.
内皮功能障碍是动脉样硬化的关键早期事件.
将Hcy与内皮功能障碍联系在一起的特定机制需要进一步阐明.

研究的目的:

研究Hcy诱导内皮功能障碍的机制.
检查CXCL10/CXCR3轴在Hcy介导的内皮损伤中的作用.
评估针对CXCL10/CXCR3轴的治疗策略.

主要方法:

在体外研究中,使用暴露于Hcy.的内皮细胞进行了实验.
在活体研究中,使用过高同胞蛋白血症 (HHcy) 的小鼠模型.
评估内皮细胞功能 (迁移,增殖,管形成) 和粘附分子表达.
对CXCL10和CXCR3表达水平的分析.
使用抗体和NBI-74330.使用CXCL10/CXCR3轴的药理学阻塞.

主要成果:

Hcy显著损害了内皮细胞的迁移,增殖和管形成.
Hcy对粘附分子进行上调,从而导致内皮功能障碍.
在HHcy小鼠中,血Hcy升高与血管损伤相关.
暴露于Hcy会增加CXCL10和CXCR3的表达在体外和体内.
阻断CXCL10/CXCR3轴可以改善Hcy诱导的内皮功能障碍.

结论:

CXCL10/CXCR3轴是Hcy诱导的内皮功能障碍的关键调解器.
向CXCL10/CXCR3通路代表了与高homocysteinemia相关的心血管疾病的潜在治疗策略.
这项研究为 Hcy 相关的血管病理背后的分子机制提供了新的见解.

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