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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

SARS-CoV-2 receptor is co-expressed with elements of the kinin-kallikrein, renin-angiotensin and coagulation systems in alveolar cells

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Author(s):
Sidarta-Oliveira, Davi [1, 2] ; Jara, Carlos Poblete [1, 3] ; Ferruzzi, Adriano J. [4, 5] ; Skaf, Munir S. [4, 5] ; Velander, William H. [6] ; Araujo, Eliana P. [1, 3] ; Velloso, Licio A. [1]
Total Authors: 7
Affiliation:
[1] Univ Estadual Campinas, Inst Biol, Obes & Comorbid Res Ctr, Lab Cell Signaling, Bloco Z, Campus Univ Zeferino Vaz, BR-13083864 Campinas, SP - Brazil
[2] Univ Estadual Campinas, Sch Med Sci, Phys Scientist Grad Program, Campinas - Brazil
[3] Univ Estadual Campinas, Nursing Sch, Campinas - Brazil
[4] Univ Estadual Campinas, Inst Chem, Campinas - Brazil
[5] Univ Estadual Campinas, Ctr Comp Engn & Sci, Campinas - Brazil
[6] Univ Nebraska, Dept Chem & Biomol Engn, Lincoln, NE 68583 - USA
Total Affiliations: 6
Document type: Journal article
Source: SCIENTIFIC REPORTS; v. 10, n. 1 NOV 11 2020.
Web of Science Citations: 12
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 similar to 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. (AU)

FAPESP's process: 13/08293-7 - CCES - Center for Computational Engineering and Sciences
Grantee:Munir Salomao Skaf
Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 13/07607-8 - OCRC - Obesity and Comorbidities Research Center
Grantee:Licio Augusto Velloso
Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC