SARS-CoV-2 receptor is co-expressed with elements of the kinin-kallikrein, renin-angiotensin and coagulation systems in alveolar cells.
Sci Rep
; 10(1): 19522, 2020 11 11.
Article
in English
| MEDLINE | ID: covidwho-920619
ABSTRACT
SARS-CoV-2, the pathogenic agent of COVID-19, employs angiotensin converting enzyme-2 (ACE2) as its cell entry receptor. Clinical data reveal that in severe COVID-19, SARS-CoV-2 infects the lung, leading to a frequently lethal triad of respiratory insufficiency, acute cardiovascular failure, and coagulopathy. Physiologically, ACE2 plays a role in the regulation of three systems that could potentially be involved in the pathogenesis of severe COVID-19 the kinin-kallikrein system, resulting in acute lung inflammatory edema; the renin-angiotensin system, promoting cardiovascular instability; and the coagulation system, leading to thromboembolism. Here we assembled a healthy human lung cell atlas meta-analysis with ~ 130,000 public single-cell transcriptomes and show that key elements of the bradykinin, angiotensin and coagulation systems are co-expressed with ACE2 in alveolar cells and associated with their differentiation dynamics, which could explain how changes in ACE2 promoted by SARS-CoV-2 cell entry result in the development of the three most severe clinical components of COVID-19.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Pulmonary Alveoli
/
Renin-Angiotensin System
/
Blood Coagulation
/
Kallikrein-Kinin System
/
Peptidyl-Dipeptidase A
/
Gene Expression Profiling
/
Betacoronavirus
Type of study:
Prognostic study
/
Reviews
Limits:
Humans
Language:
English
Journal:
Sci Rep
Year:
2020
Document Type:
Article
Affiliation country:
S41598-020-76488-2
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