COVID-19: ACE2centric Infective Disease?
Hypertension
; 76(2): 294-299, 2020 08.
Article
in English
| MEDLINE | ID: covidwho-457026
ABSTRACT
Diffuse pulmonary inflammation, endothelial inflammation, and enhanced thrombosis are cardinal features of coronavirus disease 2019 (COVID-19), the disease caused by the severe acute respiratory syndrome coronavirus 2. These features are reminiscent of several adverse reactions triggered by angiotensin II and opposed by angiotensin1-7, in many experimental models. Severe acute respiratory syndrome coronavirus 2 binds to ACE2 (angiotensin-converting enzyme 2) receptors and entries into the cell through the fusion of its membrane with that of the cell. Hence, it downregulates these receptors. The loss of ACE2 receptor activity from the external site of the membrane will lead to less angiotensin II inactivation and less generation of antiotensin1-7. In various experimental models of lung injury, the imbalance between angiotensin II overactivity and of antiotensin1-7 deficiency triggered inflammation, thrombosis, and other adverse reactions. In COVID-19, such imbalance could play an important role in influencing the clinical picture and outcome of the disease. According to this line of thinking, some therapeutic approaches including recombinant ACE2, exogenous angiotensin1-7, and angiotensin receptor blockers seem particularly promising and are being actively tested.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Pneumonia, Viral
/
Renin-Angiotensin System
/
Angiotensin-Converting Enzyme Inhibitors
/
Coronavirus Infections
/
Angiotensin Receptor Antagonists
/
Betacoronavirus
Type of study:
Observational study
/
Prognostic study
Limits:
Humans
Language:
English
Journal:
Hypertension
Year:
2020
Document Type:
Article
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