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新型冠状病毒肺炎凝血病的机制仍是个难以捉摸的问题吗？

Is the mechanism of COVID-19 coagulopathy still a rabbit's hole?

作者信息

Rajan Ashna, Thirunavukkarasu Ganesh Keshav, Lockey Richard F, Kolliputi Narasaiah

机构信息

Division of Geriatrics Medicine, Brown University Alpert School of Medicine, Providence, RI, 02903, USA.

Division of Cardiovascular Medicine, Department of Internal Medicine, State University of New York-Downstate Medical Center, Brooklyn, NY, 11203, USA.

出版信息

J Cell Commun Signal. 2022 Mar;16(1):1-3. doi: 10.1007/s12079-021-00613-7. Epub 2021 Jun 2.

DOI:10.1007/s12079-021-00613-7
PMID:34076828
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8170857/
Abstract

The pathophysiology of COVID-19 is an enigma with its severity often determined by the extent of coagulopathy. Several regulatory pathways targeted by the SARS-CoV-2 include the renin-angiotensin system, von Willebrand Factor, and most importantly, the complement pathway. This article discusses these pathways to help design potential future therapies.

摘要

新冠病毒病（COVID-19）的病理生理学是一个谜，其严重程度通常由凝血病的程度决定。严重急性呼吸综合征冠状病毒2（SARS-CoV-2）靶向的几个调节途径包括肾素-血管紧张素系统、血管性血友病因子，最重要的是补体途径。本文讨论这些途径，以帮助设计未来可能的治疗方法。

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本文引用的文献

1
ACE2: Evidence of role as entry receptor for SARS-CoV-2 and implications in comorbidities.ACE2：作为 SARS-CoV-2 进入受体的证据及其在合并症中的意义。
Elife. 2020 Nov 9;9:e61390. doi: 10.7554/eLife.61390.
2
COVID-19: what the clinician should know about post-mortem findings.新型冠状病毒肺炎：临床医生应了解的尸检结果
Intensive Care Med. 2021 Jan;47(1):86-89. doi: 10.1007/s00134-020-06302-0. Epub 2020 Nov 3.
3
ACE2, COVID-19 Infection, Inflammation, and Coagulopathy: Missing Pieces in the Puzzle.血管紧张素转换酶2、新型冠状病毒肺炎感染、炎症与凝血病：拼图中缺失的部分
Front Physiol. 2020 Oct 6;11:574753. doi: 10.3389/fphys.2020.574753. eCollection 2020.
4
Association between ABO blood groups and COVID-19 infection, severity and demise: A systematic review and meta-analysis.ABO 血型与 COVID-19 感染、严重程度和死亡的关联：系统评价和荟萃分析。
Infect Genet Evol. 2020 Oct;84:104485. doi: 10.1016/j.meegid.2020.104485. Epub 2020 Jul 30.
5
The renin-angiotensin system: An integrated view of lung disease and coagulopathy in COVID-19 and therapeutic implications.肾素-血管紧张素系统：COVID-19 中肺部疾病和凝血功能障碍的综合观点及治疗意义。
J Exp Med. 2020 Aug 3;217(8). doi: 10.1084/jem.20201000.
6
COVID-19 cytokine storm: The anger of inflammation.COVID-19 细胞因子风暴：炎症的愤怒。
Cytokine. 2020 Sep;133:155151. doi: 10.1016/j.cyto.2020.155151. Epub 2020 May 30.
7
Coagulation abnormalities and thrombosis in patients with COVID-19.新型冠状病毒肺炎患者的凝血异常与血栓形成
Lancet Haematol. 2020 Jun;7(6):e438-e440. doi: 10.1016/S2352-3026(20)30145-9. Epub 2020 May 11.
8
Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: A report of five cases.严重 COVID-19 感染发病机制中的补体相关微血管损伤和血栓形成：五例报告。
Transl Res. 2020 Jun;220:1-13. doi: 10.1016/j.trsl.2020.04.007. Epub 2020 Apr 15.
9
Corrigendum: Critical Role of Alternative M2 Skewing in miR-155 Deletion-Mediated Protection of Colitis.勘误：替代性M2极化在miR-155缺失介导的结肠炎保护中的关键作用。
Front Immunol. 2020 Feb 13;10:3153. doi: 10.3389/fimmu.2019.03153. eCollection 2019.
10
Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia.异常的凝血参数与新型冠状病毒肺炎患者的预后不良有关。
J Thromb Haemost. 2020 Apr;18(4):844-847. doi: 10.1111/jth.14768. Epub 2020 Mar 13.