自主代谢重编程和氧化应激是急性心肌梗塞中内皮功能障碍的特征
Erika Zodda1,2,3, Olga Tura-Ceide4,5,6, Nicholas L Mills7
1Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain.
eLife
|November 28, 2023
概括
在急性心肌梗塞 (AMI) 中,内皮细胞 (EC) 功能障碍涉及代谢变化. 新的研究表明,AMI衍生的ECs表现出改变的葡萄糖代谢和增加的氧化应激,有助于EC功能障碍.
科学领域:
- 心血管生物学 心血管生物学
- 细胞的新陈代谢
- 氧化压力研究研究 氧化压力研究
背景情况:
- 内皮细胞 (EC) 功能障碍在急性冠状动脉综合征中至关重要.
- 了解细胞自主机制需要合适的EC模型.
- 氧化应激在EC功能障碍中起着重要作用.
研究的目的:
- 研究急性心肌梗塞 (AMI) 中EC功能障碍的细胞自主代谢决定因素.
- 从AMI患者标本中获得的内皮细胞的特征.
主要方法:
- 从AMI患者的血栓切除样本 (AMIECs) 中生成的内皮细胞.
- 进行了表型特征 (生长,迁移,管体生成).
- 进行了代谢分析,包括ROS,谷氨,葡萄糖消耗,乳酸生产,酶活性 (PFKFB3,PFKFB4,G6PD,GLS) 和线粒体膜潜力.
主要成果:
- AMIECs显示生长受损,迁移和管道发生.
- AMIECs表现出活性氧物种 (ROS) 和谷氨的增加,葡萄糖消耗减少和乳酸盐产量高.
- 代谢转变包括上调的PFKFB4,G6PD和GLS,这表明酸途径和谷氨酸溶解激活.
- 升高的线粒体膜潜力和ROS表明了与线粒体活性相结合.
结论:
- 在AMIEC中,高线粒体质子合驱动ROS的产生.
- 酸和谷氨酸溶解途径通过谷氨合成平衡ROS.
- 这些代谢变化代表了一种主要的,细胞自主缺陷,导致AMI中的EC功能障碍.
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