在严重的COVID-19之后,肺内皮细胞中的内皮细胞激活和氧化应激
Zohreh Arab1, Seyed Abdolrahim Rezaee2, Fatemeh Sadat Mohammadi2
1Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Journal of thrombosis and thrombolysis
|October 5, 2025
概括
SARS-CoV-2 感染会导致内皮功能障碍,增加血栓形成的风险. 病毒进化改变了关键的内皮分子,影响了免疫反应,导致了严重的COVID-19结果.
科学领域:
- 心血管生物学 心血管生物学
- 传染性疾病 传染性疾病
- 分子生物学分子生物学
背景情况:
- 由SARS-CoV-2引起的COVID-19感染与内皮功能障碍有关.
- 内皮功能障碍涉及炎症路径,氧化应激和血管平衡破坏.
- 粘附分子 (ICAM-1,VCAM-1) 的升高调节和威尔布兰德因子 (vWF) 的增加有助于血管炎症和血栓形成风险.
研究的目的:
- 在SARS-CoV-2演化 (SCA和SCO波) 期间调查宿主肺内皮的变化.
- 评估SARS-CoV-2变种对内皮功能的直接影响.
- 评估参与免疫细胞招募和血管平衡的关键内皮细胞分子.
主要方法:
- 对来自COVID-19患者和对照组的支气管支气管洗液 (BALF) 样本的分析.
- 使用RT-qPCR和西式斑点测试对内皮细胞分子 (iNOS,Nrf2,NOX2,vWF,ICAM-1,VCAM-1) 的量化.
- 在SARS-CoV-2阿尔法 (SCA) 和奥米克朗 (SCO) 波和对照波之间分子变化的比较.
主要成果:
- 与对照组相比,在严重的COVID-19患者中,ICAM-1,VCAM-1和vWF的升级.
- 在Omicron波期间,诱导性氧化合成酶 (iNOS) 基因表达显著增加.
- 在SCA和SCO波中观察到NOX2的增加和Nrf2表达的减少.
结论:
- 与宿主共同进化的SARS-CoV-2导致内皮细胞功能障碍.
- 破坏内皮功能会影响免疫细胞的招募,并可能导致局部血管功能障碍.
- 向内皮分子可能为COVID-19提供治疗策略,并预防全身内皮功能障碍.
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