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内皮TERT驱动与冠状动脉疾病相关的微血管表型

Erin C Birch^1,2, Yoshinori Nishijima^1,2, Shelby N Hader^1,2

¹Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.

American journal of physiology. Heart and circulatory physiology

|June 13, 2025

概括

端粒酶逆转录酶 (TERT) 的内皮细胞特异性淘汰导致内皮功能障碍. 这损害了氧化 (NO) 介导的扩张,并促进了微容器中的多氧化 (H2O2) 介导的病态扩张.

科学领域:

心血管生物学心血管生物学
内皮细胞功能内皮细胞功能
分子医学是分子医学.

背景情况:

微血管内皮功能障碍预测动脉样硬化心脏事件.
在冠状动脉疾病 (CAD) 中,血管扩张从氧化 (NO) 转移到线粒体衍生的过氧化 (H2O2).
端粒酶逆转录酶 (TERT) 通常可以防止线粒体的活性氧物种增加,并促进NO介导的扩张.

研究的目的:

测试是否敲除内皮细胞 (EC) 特定的TERT会导致小鼠内皮功能障碍.
研究EC-TERT缺陷对微血管血管扩张机制的影响.

主要方法:

从EC特异性TERT淘汰赛 (KO) 和对照小鼠中分离的中腔动脉.
通过视频肌图学评估流媒体扩张 (FMD) 和乙胆 (ACh) 诱导的扩张.
评估了对Papaverine的平滑肌肉依赖扩张.

主要成果:

与对照组相比,EC-TERT KO小鼠的口病和ACH诱导扩张显著减少.
在EC-TERT KO小鼠中,扩张从NO介导转向混合NO/H2O2介导机制.
在EC-TERT KO小鼠中,帕帕维林对平滑肌肉依赖的血管扩张保持不变.

结论:

内皮细胞特异性TERT缺陷足以诱导内皮功能障碍.
失去EC-TERT会触发从NO介导的血管扩张到H2O2介导的血管扩张的病态转变.
内皮细胞中的TERT对于维持生理NO依赖的微血管功能至关重要.

关键词:

内皮细胞是内皮细胞.微循环是一种微循环.端粒酶的使用方法端粒酶逆转录酶的作用

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