Linking ACE2 and angiotensin II to pulmonary immunovascular dysregulation in SARS-CoV-2 infection.
Int J Infect Dis
; 101: 42-45, 2020 Dec.
Article
in English
| MEDLINE | ID: covidwho-779011
ABSTRACT
Angiotensin-converting enzyme 2 (ACE2) is the receptor of the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the coronavirus disease 2019 (COVID-19) pandemic. ACE2 has been shown to be down-regulated during coronaviral infection, with implications for circulatory homeostasis. In COVID-19, pulmonary vascular dysregulation has been observed resulting in ventilation perfusion mismatches in lung tissue, causing profound hypoxemia. Despite the loss of ACE2 and raised circulating vasoconstrictor angiotensin II (AngII), COVID-19 patients experience a vasodilative vasculopathy. This article discusses the interplay between the immune system and pulmonary vasculature and how SARS-CoV-2-mediated ACE2 disruption and AngII may contribute to the novel vascular pathophysiology of COVID-19.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Vascular Diseases
/
Angiotensin II
/
Angiotensin-Converting Enzyme 2
/
SARS-CoV-2
/
COVID-19
/
Lung
Topics:
Long Covid
Limits:
Humans
Language:
English
Journal:
Int J Infect Dis
Journal subject:
Communicable Diseases
Year:
2020
Document Type:
Article
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