蛋白S在COVID-19中的失调

IF 2.2 4区 医学 Q3 HEMATOLOGY
Martha M.S. Sim , Jeremy P. Wood
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引用次数: 2

摘要

冠状病毒病2019 (COVID-19)与血栓形成风险增加广泛相关,有许多不同的机制被提出。其中一种机制是获得性蛋白S (PS)缺乏,PS是一种血浆蛋白,调节凝血和炎症过程,包括补体激活和efferocytosis。获得性PS缺乏症在严重病毒感染患者中很常见,在COVID-19的多项研究中都有报道。这种缺乏可能是由于蛋白质的消耗、降解或清除,合成减少,或PS与其他血浆蛋白结合,从而阻断其抗凝血活性。本文就PS的功能、COVID-19患者获得性PS缺乏的证据、PS缺乏的潜在机制以及这些机制可能在COVID-19中发生的证据进行综述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Dysregulation of Protein S in COVID-19

Dysregulation of Protein S in COVID-19

Dysregulation of Protein S in COVID-19

Dysregulation of Protein S in COVID-19

Coronavirus Disease 2019 (COVID-19) has been widely associated with increased thrombotic risk, with many different proposed mechanisms. One such mechanism is acquired deficiency of protein S (PS), a plasma protein that regulates coagulation and inflammatory processes, including complement activation and efferocytosis. Acquired PS deficiency is common in patients with severe viral infections and has been reported in multiple studies of COVID-19. This deficiency may be caused by consumption, degradation, or clearance of the protein, by decreased synthesis, or by binding of PS to other plasma proteins, which block its anticoagulant activity. Here, we review the functions of PS, the evidence of acquired PS deficiency in COVID-19 patients, the potential mechanisms of PS deficiency, and the evidence that those mechanisms may be occurring in COVID-19.

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来源期刊
CiteScore
4.20
自引率
0.00%
发文量
42
审稿时长
35 days
期刊介绍: Best Practice & Research Clinical Haematology publishes review articles integrating the results from the latest original research articles into practical, evidence-based review articles. These articles seek to address the key clinical issues of diagnosis, treatment and patient management. Each issue follows a problem-orientated approach which focuses on the key questions to be addressed, clearly defining what is known and not known, covering the spectrum of clinical and laboratory haematological practice and research. Although most reviews are invited, the Editor welcomes suggestions from potential authors.
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