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http://conacyt.repositorioinstitucional.mx/jspui/handle/1000/8768| SARS-CoV-2 receptor is co-expressed with elements of the kinin-kallikrein, renin-angiotensin and coagulation systems in alveolar cells | |
| Davi Sidarta-Oliveira Carlos Poblete Jara Adriano Jose Ferruzzi Munir Skaf William Velander Eliana Pereira Araujo Licio Velloso | |
| Acceso Abierto | |
| Atribución-NoComercial-SinDerivadas | |
| https://doi.org/10.1101/2020.06.02.20120634 | |
| https://www.medrxiv.org/content/10.1101/2020.06.02.20120634v2 | |
| 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. | |
| bioRxiv | |
| 14-06-2020 | |
| Preimpreso | |
| Inglés | |
| Público en general | |
| VIRUS RESPIRATORIOS | |
| Versión publicada | |
| publishedVersion - Versión publicada | |
| Aparece en las colecciones: | Materiales de Consulta y Comunicados Técnicos |
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