患有ST升高心肌梗塞和高C反应蛋白水平的患者的红细胞诱导内皮功能障碍
John Tengbom1, Rawan Humoud1, Eftychia Kontidou1
1Division of Cardiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
American journal of physiology. Heart and circulatory physiology
|October 11, 2024
概括
发炎的ST升高心肌梗塞 (STEMI) 患者的红细胞导致内皮功能障碍. 这种功能障碍涉及酶1和氧化应激的增加,可以通过抑制这些因素来逆转.
科学领域:
- 心血管生物学 心血管生物学
- 血液学 血液学 血液学
- 血管医学 血管医学
背景情况:
- 内皮功能障碍是血管炎症的早期迹象,也是冠状动脉疾病和心肌梗塞的关键因素.
- 众所周知,红细胞 (RBC) 导致风险人群的内皮功能障碍,但它们在急性心肌梗塞 (STEMI) 中的具体作用尚不清楚.
研究的目的:
- 为了调查来自STEMI患者的红血细胞是否诱导内皮功能障碍.
- 为了确定系统性炎症在这种红细胞介导的内皮功能障碍中的作用.
主要方法:
- 来自STEMI患者和健康对照组的红血细胞与老鼠大动脉段进行了化.
- 评估了内皮依赖和独立的放松,酶活性和氧化应激标志物.
- 根据C反应性蛋白 (CRP) 水平,患者被分组.
主要成果:
- 来自STEMI患者的红细胞,CRP水平≥2 mg/L,内皮依赖放松受损.
- 用这些红细胞化增加了大动脉中阿基因酶1的表达和活性氧物种 (ROS).
- 阿基纳酶抑制和NADPH氧化酶抑制减轻了内皮功能障碍.
结论:
- 患有系统性炎症的STEMI患者的红细胞诱导了ex vivo内皮功能障碍.
- 这种效应是由增加的阿基因酶1活性和氧化应激作用的介导.
- 向阿基纳酶或氧化应激通路可能为STEMI相关的内皮功能障碍提供治疗策略.
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