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Manipulation of ACE2 expression in COVID-19
SARS-CoV-2 is the virus responsible for the ongoing COVID-19 outbreak. The virus uses ACE2 receptor for viral entry. ACE2 is part of the counter-regulatory renin-angiotensin-aldosterone system and is also expressed in the lower respiratory tract along the alveolar epithelium. There is, however, sign...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BMJ Publishing Group
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7757413/ https://www.ncbi.nlm.nih.gov/pubmed/33443121 http://dx.doi.org/10.1136/openhrt-2020-001424 |
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author | Chaudhry, Farhan Lavandero, Sergio Xie, Xiang Sabharwal, Basera Zheng, Ying-Ying Correa, Ashish Narula, Jagat Levy, Phillip |
author_facet | Chaudhry, Farhan Lavandero, Sergio Xie, Xiang Sabharwal, Basera Zheng, Ying-Ying Correa, Ashish Narula, Jagat Levy, Phillip |
author_sort | Chaudhry, Farhan |
collection | PubMed |
description | SARS-CoV-2 is the virus responsible for the ongoing COVID-19 outbreak. The virus uses ACE2 receptor for viral entry. ACE2 is part of the counter-regulatory renin-angiotensin-aldosterone system and is also expressed in the lower respiratory tract along the alveolar epithelium. There is, however, significant controversy regarding the role of ACE2 expression in COVID-19 pathogenesis. Some have argued that decreasing ACE2 expression would result in decreased susceptibility to the virus by decreasing available binding sites for SARS-CoV-2 and restricting viral entry into the cells. Others have argued that, like the pathogenesis of other viral pneumonias, including those stemming from previous severe acute respiratory syndrome (SARS) viruses, once SARS-CoV-2 binds to ACE2, it downregulates ACE2 expression. Lack of the favourable effects of ACE2 might exaggerate lung injury by a variety of mechanisms. In order to help address this controversy, we conducted a literature search and review of relevant preclinical and clinical publications pertaining to SARS-CoV-2, COVID-19, ACE2, viral pneumonia, SARS, acute respiratory distress syndrome and lung injury. Our review suggests, although controversial, that patients at increased susceptibility to COVID-19 complications may have reduced baseline ACE2, and by modulating ACE2 expression one can possibly improve COVID-19 outcomes. Herein, we elucidate why and how this potential mechanism might work. |
format | Online Article Text |
id | pubmed-7757413 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BMJ Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-77574132020-12-28 Manipulation of ACE2 expression in COVID-19 Chaudhry, Farhan Lavandero, Sergio Xie, Xiang Sabharwal, Basera Zheng, Ying-Ying Correa, Ashish Narula, Jagat Levy, Phillip Open Heart Basic and Translational Research SARS-CoV-2 is the virus responsible for the ongoing COVID-19 outbreak. The virus uses ACE2 receptor for viral entry. ACE2 is part of the counter-regulatory renin-angiotensin-aldosterone system and is also expressed in the lower respiratory tract along the alveolar epithelium. There is, however, significant controversy regarding the role of ACE2 expression in COVID-19 pathogenesis. Some have argued that decreasing ACE2 expression would result in decreased susceptibility to the virus by decreasing available binding sites for SARS-CoV-2 and restricting viral entry into the cells. Others have argued that, like the pathogenesis of other viral pneumonias, including those stemming from previous severe acute respiratory syndrome (SARS) viruses, once SARS-CoV-2 binds to ACE2, it downregulates ACE2 expression. Lack of the favourable effects of ACE2 might exaggerate lung injury by a variety of mechanisms. In order to help address this controversy, we conducted a literature search and review of relevant preclinical and clinical publications pertaining to SARS-CoV-2, COVID-19, ACE2, viral pneumonia, SARS, acute respiratory distress syndrome and lung injury. Our review suggests, although controversial, that patients at increased susceptibility to COVID-19 complications may have reduced baseline ACE2, and by modulating ACE2 expression one can possibly improve COVID-19 outcomes. Herein, we elucidate why and how this potential mechanism might work. BMJ Publishing Group 2020-12-22 /pmc/articles/PMC7757413/ /pubmed/33443121 http://dx.doi.org/10.1136/openhrt-2020-001424 Text en © Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. http://creativecommons.org/licenses/by-nc/4.0/ http://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/. |
spellingShingle | Basic and Translational Research Chaudhry, Farhan Lavandero, Sergio Xie, Xiang Sabharwal, Basera Zheng, Ying-Ying Correa, Ashish Narula, Jagat Levy, Phillip Manipulation of ACE2 expression in COVID-19 |
title | Manipulation of ACE2 expression in COVID-19 |
title_full | Manipulation of ACE2 expression in COVID-19 |
title_fullStr | Manipulation of ACE2 expression in COVID-19 |
title_full_unstemmed | Manipulation of ACE2 expression in COVID-19 |
title_short | Manipulation of ACE2 expression in COVID-19 |
title_sort | manipulation of ace2 expression in covid-19 |
topic | Basic and Translational Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7757413/ https://www.ncbi.nlm.nih.gov/pubmed/33443121 http://dx.doi.org/10.1136/openhrt-2020-001424 |
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