SARS-CoV-2 receptor is co-expressed with elements of the kinin–kallikrein, renin–angiotensin and coagulation systems in alveolar cells
Autor: | William H. Velander, Adriano J. Ferruzzi, Licio A. Velloso, Munir S. Skaf, Carlos Poblete Jara, Eliana P. Araújo, Davi Sidarta-Oliveira |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Kallikrein-Kinin System Immunology Bradykinin lcsh:Medicine 030204 cardiovascular system & hematology Peptidyl-Dipeptidase A Article Pathogenesis Alveolar cells Renin-Angiotensin System 03 medical and health sciences chemistry.chemical_compound Betacoronavirus 0302 clinical medicine Renin–angiotensin system medicine Humans Receptor lcsh:Science Blood Coagulation Lung Multidisciplinary business.industry SARS-CoV-2 Gene Expression Profiling Serine Endopeptidases lcsh:R Kinin Computational biology and bioinformatics Pulmonary Alveoli 030104 developmental biology medicine.anatomical_structure chemistry Angiotensin-converting enzyme 2 lcsh:Q Angiotensin-Converting Enzyme 2 business |
Zdroj: | Scientific Reports, Vol 10, Iss 1, Pp 1-19 (2020) Scientific Reports |
ISSN: | 2045-2322 |
Popis: | 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. |
Databáze: | OpenAIRE |
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