在长期COVID中,CCL2-介导的内皮损伤导致心脏功能障碍
Dilip Thomas1,2, Chikage Noishiki1,3, Sadhana Gaddam4
1Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA.
Nature cardiovascular research
|October 14, 2024
概括
内皮细胞 (EC) 的细胞因子在长期COVID中驱动心脏功能障碍. 针对CCL2可能为这种持续性心血管并发症提供治疗策略.
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
- 免疫学 免疫学 免疫学
背景情况:
- 长期冠状病毒病 (COVID) 心脏损伤中内皮质的作用已被认可,但机制尚不清楚.
- 内皮细胞 (ECs) 对于血管健康至关重要,并且可以受到病毒感染的影响.
研究的目的:
- 阐明内皮功能障碍在长期COVID中导致心脏损伤的机制.
- 确定特定的分子介质,将内皮细胞与SARS-CoV-2感染后的心脏功能障碍联系起来.
主要方法:
- 利用患者衍生的血栓性血管组织和诱导的多能干细胞衍生的ECs (iPSC-ECs) 来建模内皮质炎.
- 开发心脏器官 (iPSC-EC和心肌细胞) 用于SARS-CoV-2暴露后的功能评估.
- 进行了单细胞染色质可访问性和基因表达概况,高通量蛋白质组学和动物模型研究.
主要成果:
- 长期COVID模型中的内皮炎显示出细胞因子上调,特别是CCL2.
- 暴露于SARS-CoV-2的心脏器官表现出CCL2.2介导的功能障碍.
- 通过氧化应激和心脏细胞中的蛋白质修饰,CCL2与"表型切换"和心脏功能障碍有关.
结论:
- 内皮细胞释放的细胞因子,特别是CCL2,是长期COVID中心脏功能障碍的关键贡献者.
- 这些发现强调了长期COVID患者血管健康监测的重要性.
- 准CCL2介导途径为长期COVID相关心脏并发症提供了潜在的治疗途径.
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