Potential role for tissue factor in the pathogenesis of hypercoagulability associated with in COVID-19
Potential role for tissue factor in the pathogenesis of hypercoagulability associated with in COVID-19
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DOI：
10.1007/s11239-020-02172-x
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发表时间：
2020-06-09
影响因子：
4
通讯作者：
Canas, Carlos A.
中科院分区：
文献类型：
--
作者：
Bautista-Vargas, Mario;Bonilla-Abadia, Fabio;Canas, Carlos A.
2019年12月，武汉出现一种新的高传染性传染病--中国。病原体被鉴定为一种新的冠状病毒，现在被称为严重急性综合征冠状病毒-2(SARS-CoV-2)。最近的研究表明，病毒S表面蛋白与宿主呼吸道上皮细胞上鉴定的I型跨膜金属羧肽酶-血管紧张素转换酶-2结合时，病毒就会进入人体。病毒可触发包括IL-6和TNF-α在内的促炎细胞因子的合成和释放，并促进ACE-2的下调，从而促进血管紧张素II(AT-II)水平的升高。肿瘤坏死因子-α和血管紧张素Ⅱ都被认为促进了血小板和巨噬细胞组织因子(TF)的过度表达。此外，与新冠肺炎相关的抗磷脂抗体的产生也可能促进转铁蛋白的增加。Tf可能是新冠肺炎血栓形成过程中的重要介质，值得进一步研究。
In December 2019, a new and highly contagious infectious disease emerged in Wuhan, China. The etiologic agent was identified as a novel coronavirus, now known as Severe Acute Syndrome Coronavirus-2 (SARS-CoV-2). Recent research has revealed that virus entry takes place upon the union of the virus S surface protein with the type I transmembrane metallo-carboxypeptidase, angiotensin converting enzyme 2 (ACE-2) identified on epithelial cells of the host respiratory tract. Virus triggers the synthesis and release of pro-inflammatory cytokines, including IL-6 and TNF-alpha and also promotes downregulation of ACE-2, which promotes a concomitant increase in levels of angiotensin II (AT-II). Both TNF-alpha and AT-II have been implicated in promoting overexpression of tissue factor (TF) in platelets and macrophages. Additionally, the generation of antiphospholipid antibodies associated with COVID-19 may also promote an increase in TF. TF may be a critical mediator associated with the development of thrombotic phenomena in COVID-19, and should be a target for future study.