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高致病性冠状病毒感染与免疫血栓形成的机制研究进展

Highly pathogenic coronavirus infection and immunothrombosis:research advances
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摘要 目的综述高致病性冠状病毒感染时免疫血栓形成机制,为临床防治提供参考。方法查阅国内外文献,从凝血功能紊乱,免疫/炎症反应失调,内皮细胞损伤/功能障碍、血小板障碍等方面综述高致病性冠状病毒导致宿主免疫血栓的致病机制。结果高致病性冠状病毒感染导致失控的免疫血栓形成与细胞因子风暴、中性粒细胞胞外陷阱形成、补体系统和肾素血管紧张素系统过度激活,内皮细胞氧化应激及糖萼损伤等有关,是造成患者重症及死亡的关键原因。结论深入研究高致病性冠状病毒感染引起免疫血栓的发病机制,开发并评估潜在的治疗干预措施,不仅可以减轻该病的急性和远期后果,对未来应对其他新发、突发感染性疾病也具有重大意义。 Objective To review the mechanism of immunethrombosis in highly pathogenic coronavirus(HPCoVs)infections and provide reference for clinical prevention and treatment.Methods Domestic and foreign literature was reviewed to outline the pathogenic mechanism of host immunethrombosis caused by Hcov in terms of coagulation disorders,immune/inflammatory disorders,endothelial cell injury/dysfunction,and platelet disorders.Results The uncontrolled immunethrombosis caused by Hcov infections was related to cytokine storm,formation of neutrophil extracellular traps,excessive activation of the complement system and renin-angiotensin system,oxidative stress of endothelial cells and glycocalyx damage,which were the leading causes of critical illness and death of patients.Conclusion An in-depth study of the pathogenesis of immunethrombosis due to highly pathogenic coronavirus infections and the development and evaluation of potential therapeutic interventions could not only mitigate the acute and long-term consequences of the disease,but also have significant implications for future responses to other emerging and emergent infectious diseases.
作者 孙绮悦 郭姗姗 赵荣华 包蕾 耿子涵 李舒冉 徐英莉 张敬升 崔晓兰 孙静 SUN Qiyue;GUO Shanshan;ZHAO Ronghua;BAO Lei;GENG Zihan;LI Shuran;XU Yingli;ZHANG Jingsheng;CUI Xiaolan;SUN Jing(Institute of Chinese Materia Medica,China Academy of Chinese Medical Sciences,Beijing 100029,China)
出处 《中国药物警戒》 2024年第3期246-252,共7页 Chinese Journal of Pharmacovigilance
基金 国家自然科学基金资助项目(82104500) 中国中医科学院科技创新工程项目(CI2021B015)。
关键词 高致病性 冠状病毒感染 免疫血栓形成 过度炎症 内皮损伤 凝血系统激活 highly pathogenic coronavirus infection immune thrombosis hyperinflammation endothelial damage coagulation system activation
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