COVID-19 Vasculopathy: Mounting Evidence for an Indirect Mechanism of Endothelial Injury.
Am J Pathol
; 191(8): 1374-1384, 2021 08.
Article
in English
| MEDLINE | ID: covidwho-1240148
ABSTRACT
Patients with coronavirus disease 2019 (COVID-19) who are critically ill develop vascular complications characterized by thrombosis of small, medium, and large vessels. Dysfunction of the vascular endothelium due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been implicated in the pathogenesis of the COVID-19 vasculopathy. Although initial reports suggested that endothelial injury was caused directly by the virus, recent studies indicate that endothelial cells do not express angiotensin-converting enzyme 2, the receptor that SARS-CoV-2 uses to gain entry into cells, or express it at low levels and are resistant to the infection. These new findings, together with the observation that COVID-19 triggers a cytokine storm capable of injuring the endothelium and disrupting its antithrombogenic properties, favor an indirect mechanism of endothelial injury mediated locally by an augmented inflammatory reaction to infected nonendothelial cells, such as the bronchial and alveolar epithelium, and systemically by the excessive immune response to infection. Herein we review the vascular pathology of COVID-19 and critically discuss the potential mechanisms of endothelial injury in this disease.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Thrombosis
/
Endothelium, Vascular
/
Cytokine Release Syndrome
/
SARS-CoV-2
/
COVID-19
Type of study:
Observational study
/
Prognostic study
Topics:
Long Covid
Limits:
Humans
Language:
English
Journal:
Am J Pathol
Year:
2021
Document Type:
Article
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