SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis
- Autores
- Delpino, María Victoria; Quarleri, Jorge Fabian
- Año de publicación
- 2020
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- After SARS-CoV-2 infection, a major complication of those who survived to COVID-19 outbreak is the development of severe lung disease leading to pulmonary fibrosis. At earliest step of virus-host cell interaction when the SARS-CoV-2 interacts with the ACE2 receptor highly expressed in pneumocytes type II, a linkage is established between the renin-angiotensin-system (RAS) and the viral pathogenesis. Within this important system, the angiotensin-converting enzyme (ACE) is deputed to the conversion of angiotensin I to angiotensin II (AngII), a potent vasoconstrictive peptide involved directly in inflammation and fibrosis development. AngII is hydrolyzed by ACE2 to Ang1-7, triggering a cascade of events that counteract fibrosis. This imbalance is known to be due to inflammatory damage. However, because ACE2 is the receptor for SARS-Cov-2, we could also speculate that the virus per se could modulate its enzymatic activity. In our opinion the wound healing pathways that mediate tissue repair after SARS-CoV-2 mediated injury, should consider managing the imbalanced ACE/ACE2 axis. We hypothesize that the heptapeptide Ang1-7 could provide novel therapeutic interventions for pulmonary fibrosis patients. Understanding how the RAS, wound healing and other pro-fibrotic pathways act after viral infection should lead to novel therapeutics in the future.
Fil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Quarleri, Jorge Fabian. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina - Materia
-
SARS-COV-2
ACE2
FIBROSIS
RENIN ANGIOTENSIN SYSTEM (RAS)
ANG1-7
COVID-19 - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/108393
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SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung FibrosisDelpino, María VictoriaQuarleri, Jorge FabianSARS-COV-2ACE2FIBROSISRENIN ANGIOTENSIN SYSTEM (RAS)ANG1-7COVID-19https://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3After SARS-CoV-2 infection, a major complication of those who survived to COVID-19 outbreak is the development of severe lung disease leading to pulmonary fibrosis. At earliest step of virus-host cell interaction when the SARS-CoV-2 interacts with the ACE2 receptor highly expressed in pneumocytes type II, a linkage is established between the renin-angiotensin-system (RAS) and the viral pathogenesis. Within this important system, the angiotensin-converting enzyme (ACE) is deputed to the conversion of angiotensin I to angiotensin II (AngII), a potent vasoconstrictive peptide involved directly in inflammation and fibrosis development. AngII is hydrolyzed by ACE2 to Ang1-7, triggering a cascade of events that counteract fibrosis. This imbalance is known to be due to inflammatory damage. However, because ACE2 is the receptor for SARS-Cov-2, we could also speculate that the virus per se could modulate its enzymatic activity. In our opinion the wound healing pathways that mediate tissue repair after SARS-CoV-2 mediated injury, should consider managing the imbalanced ACE/ACE2 axis. We hypothesize that the heptapeptide Ang1-7 could provide novel therapeutic interventions for pulmonary fibrosis patients. Understanding how the RAS, wound healing and other pro-fibrotic pathways act after viral infection should lead to novel therapeutics in the future.Fil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Quarleri, Jorge Fabian. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFrontiers Research Foundation2020-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/108393Delpino, María Victoria; Quarleri, Jorge Fabian; SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis; Frontiers Research Foundation; Frontiers in Cellular and Infection Microbiology; 10; 6-2020; 1-52235-2988CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/article/10.3389/fcimb.2020.00340/fullinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fcimb.2020.00340info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:04:30Zoai:ri.conicet.gov.ar:11336/108393instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:04:30.301CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis |
title |
SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis |
spellingShingle |
SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis Delpino, María Victoria SARS-COV-2 ACE2 FIBROSIS RENIN ANGIOTENSIN SYSTEM (RAS) ANG1-7 COVID-19 |
title_short |
SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis |
title_full |
SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis |
title_fullStr |
SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis |
title_full_unstemmed |
SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis |
title_sort |
SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis |
dc.creator.none.fl_str_mv |
Delpino, María Victoria Quarleri, Jorge Fabian |
author |
Delpino, María Victoria |
author_facet |
Delpino, María Victoria Quarleri, Jorge Fabian |
author_role |
author |
author2 |
Quarleri, Jorge Fabian |
author2_role |
author |
dc.subject.none.fl_str_mv |
SARS-COV-2 ACE2 FIBROSIS RENIN ANGIOTENSIN SYSTEM (RAS) ANG1-7 COVID-19 |
topic |
SARS-COV-2 ACE2 FIBROSIS RENIN ANGIOTENSIN SYSTEM (RAS) ANG1-7 COVID-19 |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.3 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
After SARS-CoV-2 infection, a major complication of those who survived to COVID-19 outbreak is the development of severe lung disease leading to pulmonary fibrosis. At earliest step of virus-host cell interaction when the SARS-CoV-2 interacts with the ACE2 receptor highly expressed in pneumocytes type II, a linkage is established between the renin-angiotensin-system (RAS) and the viral pathogenesis. Within this important system, the angiotensin-converting enzyme (ACE) is deputed to the conversion of angiotensin I to angiotensin II (AngII), a potent vasoconstrictive peptide involved directly in inflammation and fibrosis development. AngII is hydrolyzed by ACE2 to Ang1-7, triggering a cascade of events that counteract fibrosis. This imbalance is known to be due to inflammatory damage. However, because ACE2 is the receptor for SARS-Cov-2, we could also speculate that the virus per se could modulate its enzymatic activity. In our opinion the wound healing pathways that mediate tissue repair after SARS-CoV-2 mediated injury, should consider managing the imbalanced ACE/ACE2 axis. We hypothesize that the heptapeptide Ang1-7 could provide novel therapeutic interventions for pulmonary fibrosis patients. Understanding how the RAS, wound healing and other pro-fibrotic pathways act after viral infection should lead to novel therapeutics in the future. Fil: Delpino, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Quarleri, Jorge Fabian. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina |
description |
After SARS-CoV-2 infection, a major complication of those who survived to COVID-19 outbreak is the development of severe lung disease leading to pulmonary fibrosis. At earliest step of virus-host cell interaction when the SARS-CoV-2 interacts with the ACE2 receptor highly expressed in pneumocytes type II, a linkage is established between the renin-angiotensin-system (RAS) and the viral pathogenesis. Within this important system, the angiotensin-converting enzyme (ACE) is deputed to the conversion of angiotensin I to angiotensin II (AngII), a potent vasoconstrictive peptide involved directly in inflammation and fibrosis development. AngII is hydrolyzed by ACE2 to Ang1-7, triggering a cascade of events that counteract fibrosis. This imbalance is known to be due to inflammatory damage. However, because ACE2 is the receptor for SARS-Cov-2, we could also speculate that the virus per se could modulate its enzymatic activity. In our opinion the wound healing pathways that mediate tissue repair after SARS-CoV-2 mediated injury, should consider managing the imbalanced ACE/ACE2 axis. We hypothesize that the heptapeptide Ang1-7 could provide novel therapeutic interventions for pulmonary fibrosis patients. Understanding how the RAS, wound healing and other pro-fibrotic pathways act after viral infection should lead to novel therapeutics in the future. |
publishDate |
2020 |
dc.date.none.fl_str_mv |
2020-06 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/108393 Delpino, María Victoria; Quarleri, Jorge Fabian; SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis; Frontiers Research Foundation; Frontiers in Cellular and Infection Microbiology; 10; 6-2020; 1-5 2235-2988 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/108393 |
identifier_str_mv |
Delpino, María Victoria; Quarleri, Jorge Fabian; SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis; Frontiers Research Foundation; Frontiers in Cellular and Infection Microbiology; 10; 6-2020; 1-5 2235-2988 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/article/10.3389/fcimb.2020.00340/full info:eu-repo/semantics/altIdentifier/doi/10.3389/fcimb.2020.00340 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Frontiers Research Foundation |
publisher.none.fl_str_mv |
Frontiers Research Foundation |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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13.13397 |