在PASC患有心血管并发症的PASC患者中,持续的单细胞生物能量损伤和线粒体DNA损伤
Dilvin Semo1,2, Zornitsa Shomanova3, Jürgen Sindermann3
1Vascular Signalling, Molecular Cardiology, Department of Cardiology I, Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital Münster, 48149 Münster, Germany.
International journal of molecular sciences
|May 28, 2025
概括
免疫细胞中的线粒体功能障碍在长期COVID (SARS-CoV-2感染的急性后续) 中导致心血管问题. 长期COVID单细胞显示能量产生受损和DNA损伤,而不是直接的病毒效应,表明宿主反应是原因.
科学领域:
- 免疫学 免疫学 免疫学
- 心脏病学 心脏病学
- 线粒体生物学 线粒体生物学
- 传染病病理生理学 传染病病理生理学
背景情况:
- 心血管并发症在SARS-CoV-2感染的急性后续 (PASC) 中很常见,但潜在的机制尚不清楚.
- 免疫细胞中的线粒体功能障碍越来越多地与PASC的持续性心脏问题有关.
- 这项研究侧重于CD14++单细胞,研究它们的生物能功能,线粒体DNA (mtDNA) 完整性和长期COVID患者的氧化应激反应.
研究的目的:
- 为了研究长期COVID患者的CD14++单细胞中的线粒体功能障碍,这些患者有心血管症状.
- 评估这些单细胞中的生物能量损伤,mtDNA损伤和氧化应激适应.
- 为了确定SARS-CoV-2尖端蛋白是否直接导致健康单细胞中的这些线粒体缺陷.
主要方法:
- 从14名长期COVID患者和10名年龄相匹配的对照组中分离出CD14++单细胞.
- 使用海马分析仪和FACS.评估线粒体功能 (呼吸,质子泄漏,ROS).
- 测量了线粒体膜潜力 (TMRE测定) 和mtDNA完整性 (qPCR);健康单细胞暴露在SARS-CoV-2尖端蛋白中进行比较.
主要成果:
- 长期COVID单细胞表现出基本和最大呼吸受损,并且在氧化应激下显著减少了备用呼吸能力.
- 这些单细胞显示了的质子泄漏,矛盾地减少了ROS积累,并提高了线粒体膜潜力.
- 在长期COVID单细胞中观察到严重的mtDNA枯竭和特定区域的损伤;单独的SARS-CoV-2尖端蛋白不能复制这些缺陷.
结论:
- 长期COVID中的线粒体功能障碍是由不适应的宿主反应驱动的,而不是直接的病毒毒性,其特点是生物能量失败和基因组不稳定.
- 单细胞中线粒体功能受损和mtDNA损伤与PASC中心脏衰竭和运动不耐受等心血管症状相关.
- 线粒体弹性代表了长期COVID心血管并发症的治疗目标,需要进一步研究宿主导的机制.
关键词:
在CD14++单细胞中.生物能源特征 生物能源特征心脏衰竭是因为心脏衰竭.长时间COVID综合征单细胞线粒体功能障碍 单细胞线粒体功能障碍导致mtDNA损伤.氧化应激适应适应 氧化应激适应反应性氧物种 (ROS) 是一种反应性氧物种.海马分析分析海马分析更多相关视频
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