Vasculopathy and Coagulopathy Associated with SARS-CoV-2 Infection

Cells

Giovanna Tosato¹  Hidetaka Ohnuki¹  Nazzarena Labò² 

[1] Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA;Viral Oncology Section, AIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Leidos Biochemical Research Inc., Frederick, MD 21702, USA;

关键词: COVID-19;    SARS-CoV-2;    ACE2;    inflammatory cytokines;    vasculopathy;    vascular inflammation;   

DOI  :  10.3390/cells9071583

来源: DOAJ

【 摘 要 】

The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in > 500,000 deaths worldwide, including > 125,000 deaths in the U.S. since its emergence in late December 2019 and June 2020. Neither curative anti-viral drugs nor a protective vaccine is currently available for the treatment and prevention of COVID-19. Recently, new clinical syndromes associated with coagulopathy and vasculopathy have emerged as a cause of sudden death and other serious clinical manifestations in younger patients infected with SARS-CoV-2 infection. Angiotensin converting enzyme 2 (ACE2), the receptor for SARS-CoV-2 and other coronaviruses, is a transmembrane protein expressed by lung alveolar epithelial cells, enterocytes, and vascular endothelial cells, whose physiologic role is to induce the maturation of angiotensin I to generate angiotensin 1-7, a peptide hormone that controls vasoconstriction and blood pressure. In this review, we provide the general context of the molecular and cellular mechanisms of SARS-CoV-2 infection with a focus on endothelial cells, describe the vasculopathy and coagulopathy syndromes in patients with SARS-CoV-2, and outline current understanding of the underlying mechanistic aspects.

【 授权许可】

Unknown