血管新陈代谢的年龄相关重编程损害了内皮细胞对炎症诱导的内皮功能障碍的弹性
Agnieszka Karaś1, Elżbieta Buczek1, Janusz Pyka1
1Jagiellonian University, Jagiellonian Centre for Experimental Therapeutics, Krakow, Poland.
Free radical biology & medicine
|December 28, 2025
概括
衰老通过改变血管代谢而加剧内皮功能障碍. 在老年小鼠中,炎症将细胞能量生产转移到酸通路,损害血管功能.
科学领域:
- 血管生物学 血管生物学
- 代谢调节 代谢调节 代谢调节
- 衰老研究研究 衰老研究
背景情况:
- 内皮功能障碍与血管炎症和衰老有关.
- 细胞生物能学在与年龄相关的内皮细胞对炎症的抵抗力中的作用尚不清楚.
研究的目的:
- 为了研究IL-1β诱导的炎症如何影响血管新陈代谢和内皮功能,在老年与年轻小鼠的大动脉.
- 描述炎症期间老年血管系统中代谢重编程的特征.
主要方法:
- 外体线筋图和电子磁共振光谱 (EPR) 用于内皮功能和NO生产.
- 对线粒体呼吸和糖解的海马细胞外流量分析.
- 13C-葡萄糖流量,高能酸盐测量和药理抑制研究.
主要成果:
- 较老的小鼠表现出更严重的IL-1β诱导的内皮功能障碍.
- 年轻的大动脉表现出线粒体呼吸和糖解的增加;老大动脉显示出转向酸通路 (PPP).
- 抑制PPP在老年小鼠中恢复了内皮功能,表明其不适应性作用.
结论:
- 年龄相关的代谢重编程会影响血管对炎症的反应.
- 在老年的大动脉中,受损的pyruvate氧化和TCA流量有助于内皮功能障碍.
- 线粒体呼吸,而不是糖解,对于NO依赖的血管扩张至关重要.
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