在COVID-19中,SARS-CoV-2尖端蛋白诱导的炎症是COVID-19中的前节律失常的基础
Louisa Mezache1, Andrew Soltisz2, Esmerina Tili3
1College of Pharmacy , The Ohio State University , 2255 Kenny Rd, Columbus, OH, 43210, USA. mezache.2@osu.edu.
Scientific reports
|September 30, 2025
概括
SARS-CoV-2 尖端蛋白质可以通过引发炎症和血管损伤而导致心脏节律失常,而不是直接感染心脏. 这种炎症反应会破坏心脏细胞连接,导致COVID-19患者心律问题.
科学领域:
- 心脏病学 心脏病学
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
背景情况:
- 冠状病毒疾病2019 (COVID-19) 在患者中显著增加心律失常风险,特别是心房动 (AF).
- 在COVID-19中心脏并发症范围从非ICU患者的2%到非幸存者的59%.
- 虽然心脏中的ACE2表达表明病毒感染,但之前的研究发现致命的COVID-19心脏组织中存在炎症标志物和血管损伤,而不是直接的SARS-CoV-2感染.
研究的目的:
- 调查SARS-CoV-2尖端蛋白的炎症反应是否足以引起心房失常.
- 探索由尖端蛋白暴露引起的结构和功能性心脏变化.
主要方法:
- 野生型 (WT) 小鼠接受了SARS-CoV-2尖端蛋白的单次静脉注射.
- 实体心电图 (ECG) 用于评估心脏电活动和心律失常负担.
- 进行了免疫组织化学检查,以评估炎症标志物,血管损伤以及关键心脏蛋白 (连xin-43 和 NaV1.5) 在间隔性盘中的定位.
主要成果:
- 与对照组相比,注射尖端蛋白的小鼠表现出心房失常负担显著增加.
- 在注射小鼠的心脏中观察到炎症标志物升高和血管损伤的证据.
- 在心房中发现了间歇性盘超结构的破坏和连xin-43 和 NaV1.5 的错位.
结论:
- 由SARS-CoV-2尖端蛋白引起的炎症性侮辱,导致血管泄漏,足以诱导心房失常.
- 这些发现表明,炎症,而不是直接的病毒感染,是严重的COVID-19中心脏功能障碍和心律失常的基础.
- 观察到的间隙盘的破坏和蛋白质错位导致炎症性侵伤后的心律失常基质.
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