SARS-CoV-2 receptor is co-expressed with elements of the kinin-kallikrein, renin-angiotensin and coagulation systems in alveolar cells
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 analyzed ~130,000 human lung single-cell transcriptomes and show that key elements of the kinin-kallikrein, renin-angiotensin and coagulation systems are co-expressed with ACE2 in alveolar cells, 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..
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Preprint| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
bioRxiv.org - (2024) vom: 30. Apr. Zur Gesamtaufnahme - year:2024 |
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| Sprache: |
Englisch |
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| Beteiligte Personen: |
Sidarta-Oliveira, Davi [VerfasserIn] |
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| doi: |
10.1101/2020.06.02.20120634 |
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| PPN (Katalog-ID): |
XBI018073654 |
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| 520 | |a 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 analyzed ~130,000 human lung single-cell transcriptomes and show that key elements of the kinin-kallikrein, renin-angiotensin and coagulation systems are co-expressed with ACE2 in alveolar cells, 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. | ||
| 650 | 4 | |a Biology |7 (dpeaa)DE-84 | |
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| 700 | 1 | |a Jara, Carlos Poblete |e verfasserin |0 (orcid)0000-0001-5444-721X |4 aut | |
| 700 | 1 | |a Ferruzzi, Adriano J. |e verfasserin |0 (orcid)0000-0002-1268-7132 |4 aut | |
| 700 | 1 | |a Skaf, Munir S. |e verfasserin |0 (orcid)0000-0001-7485-1228 |4 aut | |
| 700 | 1 | |a Velander, William H. |e verfasserin |0 (orcid)0000-0002-8020-5174 |4 aut | |
| 700 | 1 | |a Araujo, Eliana P. |e verfasserin |0 (orcid)0000-0002-7539-8477 |4 aut | |
| 700 | 1 | |a Velloso, Licio A. |e verfasserin |0 (orcid)0000-0002-4806-7218 |4 aut | |
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