促炎性细胞因子在COVID-19中驱动心脏毒性
Maria Colzani1,2, Johannes Bargehr1,2, Federica Mescia2,3
1Wellcome - MRC Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Puddicombe Way, CB2 0AW Cambridge, UK.
在COVID-19患者中.
科学领域:
- 心脏病学 心脏病学
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
背景情况:
- 在COVID-19患者中,心脏参与是常见的,影响疾病结果.
- 直接的病毒影响和全身炎症有助于心脏损伤.
- 血清诱导的心脏毒性是COVID-19中研究不足的机制.
研究的目的:
- 调查COVID-19中心脏毒性的血清学驱动因素.
- 评估COVID-19患者血清对心肌细胞的影响.
- 确定涉及COVID-19相关心脏损伤的炎症途径.
主要方法:
- 开发了一种使用人类胚胎干细胞衍生的心肌细胞的生物试验.
- 暴露于COVID-19和ARDS患者血清中的心肌细胞.
- 通过大量RNA测序分析了心肌细胞活力,炎症性细胞因子水平和基因表达.
主要成果:
- COVID-19患者血清降低了心肌细胞活力,独立于病毒转导.
- 来自严重COVID-19病例的血清显示出更大的心脏毒性,与炎症性细胞因子 (IL-6,TNF-α) 和免疫细胞变化相关.
- 阻断IL-6和TNF-α部分恢复了心肌细胞的活力.
- 血清诱导的内皮激活和前凝剂状态,而不会影响内皮细胞活力.
结论:
- 在COVID-19血清中的炎症性细胞因子对心血管损伤有显著的贡献.
- 在受到COVID-19血清影响的心肌细胞中确定了特定的分子通路.
- 严重的COVID-19血清概况表明心脏并发症的潜在治疗点.
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