在COVID-19感染后,蛋白质学对热素升高的见解
Anna Kamdar1,2, Daniel Tze Yee Ang1,2, Kenneth Mangion1,2
1Department of Cardiology, Golden Jubilee National Hospital, Clydebank, UK.
像COVID-19这样的病毒感染中心脏热素-I的升高可能表明系统性血管损伤,而不仅仅是心脏损伤. 了解这种机制可以改善生物标志物的解释,并指导未来的治疗方法.
科学领域:
- 心脏病学 心脏病学
- 传染性疾病 传染性疾病
- 蛋白质组学是指蛋白质组学.
背景情况:
- 心脏托罗邦素-I的升高在急性病毒感染中很常见,包括COVID-19.
- 在没有明显的心肌损伤的情况下,热素升高的原因尚不清楚.
- 这在临床实践中构成了诊断挑战.
研究的目的:
- 为了研究住院COVID-19患者中热素升高的机制.
- 为了将蛋白质组数据与心脏生物标志物和成像相关联.
- 为了探索潜在的系统性血管损伤作为原因.
主要方法:
- 对267名COVID-19患者进行的前性多中心CISCO-19研究 (NCT04403607).
- 包括血蛋白质组学 (SOMAscan V.4.1),心血管MRI和临床生物标志物.
- 在入学时和感染后28-60天进行多系统评估.
主要成果:
- 13.2%的参与者表示心肌炎的可能性很高.
- 观察到过高的高灵敏性托罗邦尼-I水平,与性别特定的值.
- 顺肌肉中肌酸光链蛋白的下调,与托罗邦I水平相关.
结论:
- 在COVID-19中热素升高可能意味着系统性血管损伤.
- 识别血管损伤可以改进病毒性疾病中的心脏生物标志物解释.
- 这一发现支持在未来的治疗策略中研究血管损伤.
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