COVID-19促进内皮功能障碍和血栓发生:促炎性细胞因子/SGLT2促氧化途径的作用
Ali Mroueh1, Walaa Fakih1, Adrien Carmona2
1INSERM (French National Institute of Health and Medical Research), UMR 1260, Regenerative Nanomedicine, FMTS, Strasbourg, France.
Journal of thrombosis and haemostasis : JTH
|October 5, 2023
概括
COVID-19通过SGLT2过度表达引起内皮功能障碍,增加心血管风险. 作为SGLT2抑制剂的empagliflozin在恢复COVID-19患者的血管健康方面表现有前途.
科学领域:
- 心血管医学 心血管医学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- COVID-19与心血管并发症的增加有关.
- 细胞因子在内皮损伤中发挥作用,但机制尚不清楚.
研究的目的:
- 为了调查COVID-19炎症是否通过SGLT2过度表达导致内皮功能障碍.
- 评估empagliflozin (SGLT2抑制剂) 对这种功能障碍的保护作用.
主要方法:
- 分析了来自COVID-19患者,非COVID-19个体和健康对照者的血.
- 暴露在血中的内皮细胞 (ECs) 并测量了SGLT2表达,氧化应激和血小板激活.
- 使用了西方斑点,免疫光,qPCR和二乙染色.
主要成果:
- 在COVID-19患者中,炎症前导细胞因子 (IL-1β,IL-6,TNF-α) 的水平升高.
- COVID-19 血诱导了 EC 中 SGLT2 的上调,导致功能障碍,衰老和血小板活性增加.
- 恩帕格利弗洛辛和细胞因子中和抗体减少了这些影响.
结论:
- 在COVID-19中,促炎性细胞因子上调SGLT2,导致内皮损伤和血栓形成.
- 用empagliflozin抑制SGLT2是一种潜在的治疗策略,用于COVID-19中的血管平衡.
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