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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...

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Autores principales: Chaudhry, Farhan, Lavandero, Sergio, Xie, Xiang, Sabharwal, Basera, Zheng, Ying-Ying, Correa, Ashish, Narula, Jagat, Levy, Phillip
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2020
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.
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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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