Dysfunctional Coagulation in COVID-19: From Cell to Bedside.

Abstract:

:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), which can induce multisystem disease. Human angiotensin-converting enzyme 2 (ACE2) widely expressing in arterial and venous endothelial cells and arterial smooth muscle cells has been identified as a functional receptor for SARS-CoV-2. Dysfunction of ACE2 leads to abnormal activation of the renin-angiotensin system and a systemic endotheliitis that may relate to abnormal coagulation and sepsis. Meanwhile, innate immune response and inflammation activation participate in dysfunctional coagulation. Previous research indicated that dysfunctional coagulation was one of the important risk factors accountable for a high risk of severe disease and death in patients with COVID-19. Understanding the possible mechanisms of dysfunctional coagulation and appropriate anticoagulation therapeutic strategies are important to prevent disease deterioration and reduce fatality rates during the ongoing COVID-19 pandemic.

journal_name

Adv Ther

journal_title

Advances in therapy

authors

Wang J,Saguner AM,An J,Ning Y,Yan Y,Li G

doi

10.1007/s12325-020-01399-7

subject

Has Abstract

pub_date

2020-07-01 00:00:00

pages

3033-3039

issue

7

eissn

0741-238X

issn

1865-8652

pii

10.1007/s12325-020-01399-7

journal_volume

37

pub_type

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