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
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/108393
Acceder
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network_name_str CONICET Digital (CONICET)
spelling 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 Técnicas2025-09-29T10:23:35Zoai: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:34982025-09-29 10:23:36.088CONICET 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
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv 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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score 13.069144

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