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Cong Thanh Nguyen¹, Misako Nakayama¹, Hirohito Ishigaki¹

¹Division of Pathogenesis and Disease Regulation, Department of Pathology, Shiga University of Medical Science, Otsu, Japan.

|March 20, 2024

概括

SARS-CoV-2 感染激活了内皮细胞,影响了尼古丁胺氨酸二核酸 (NAD) 代谢. 在COVID-19患者中提升CD38的调节可能会防止有害的IL-6信号传递,这表明一个潜在的治疗点.

科学领域:

分子生物学分子生物学
免疫学免疫学免疫学
传染病的发病因子传染病的发病因子

背景情况:

感染SARS-CoV-2引发内皮细胞 (EC) 激活,导致功能障碍和内皮病变.
在SARS-CoV-2感染期间,尼古丁胺胺氨基二核酸 (NAD) 代谢在EC中发生变化.
CD38分子在炎症反应期间在NAD降解中发挥作用.

研究的目的:

为了研究SARS-CoV-2感染后的EC激活和NAD代谢变化.
为了阐明CD38在SARS-CoV-2诱导的内皮质病变中的作用.
确定COVID-19期间EC中CD38上调的功能意义.

主要方法:

在受感染的Cynomolgus中分析EC激活标记物,血管内纤维素和NAD代谢酶.
在实验室研究中,使用暴露于互白素-6 (IL-6) 跨信号的人类EC.
评估CD38mRNA表达及其对IL-6mRNA和EC亡的影响.

主要成果:

从感染后的第三天开始,在身上观察到EC激活和CD38水平的增加.
在体外,IL-6跨信号调节了人类ECs中的CD38mRNA.
CD38 mRNA沉默加剧了IL-6 mRNA上调,并在IL-6刺激下促进了EC亡.

结论:

在COVID-19患者中CD38的升级似乎对SARS-CoV-2诱导的IL-6转信号起着保护作用.
CD38调制可能是管理COVID-19相关内皮质病的治疗策略.

关键词:

CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 它们是Cynomolgus.脑内皮质变异症 (Endotheliopathy) 是一种内皮质变异症.介素-6的跨信号传递尼古丁胺胺腺因二核酸是什么这就是SARS-CoV-2病毒.

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