Functional ACE2 deficiency leading to angiotensin imbalance in the pathophysiology of COVID-19.
Rev Endocr Metab Disord
; 23(2): 151-170, 2022 04.
Article
in English
| MEDLINE | ID: covidwho-1290217
ABSTRACT
SARS-CoV-2, the virus responsible for COVID-19, uses angiotensin converting enzyme 2 (ACE2) as its primary cell-surface receptor. ACE2 is a key enzyme in the counter-regulatory pathway of the broader renin-angiotensin system (RAS) that has been implicated in a broad array of human pathology. The RAS is composed of two competing pathways that work in opposition to each other the "conventional" arm involving angiotensin converting enzyme (ACE) generating angiotensin-2 and the more recently identified ACE2 pathway that generates angiotensin (1-7). Following the original SARS pandemic, additional studies suggested that coronaviral binding to ACE2 resulted in downregulation of the membrane-bound enzyme. Given the similarities between the two viruses, many have posited a similar process with SARS-CoV-2. Proponents of this ACE2 deficiency model argue that downregulation of ACE2 limits its enzymatic function, thereby skewing the delicate balance between the two competing arms of the RAS. In this review we critically examine this model. The available data remain incomplete but are consistent with the possibility that the broad multisystem dysfunction of COVID-19 is due in large part to functional ACE2 deficiency leading to angiotensin imbalance with consequent immune dysregulation and endothelial cell dysfunction.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Angiotensins
/
Angiotensin-Converting Enzyme 2
/
COVID-19
Limits:
Humans
Language:
English
Journal:
Rev Endocr Metab Disord
Journal subject:
Endocrinology
/
Metabolism
Year:
2022
Document Type:
Article
Affiliation country:
S11154-021-09663-z
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