Pathophysiology of COVID-19: Critical Role of Hemostasis

Autores
Aparecida de Andrade, Sonia Aparecida; de Souza, Daniel Alexandre; Torres, Amarylis Lins; Ferreira Graça de Lima, Cristiane; Ebram, Matteo Celano; Celano Ebram, Rosa Maria; Schattner, Mirta Ana; Chudzinski Tavassi, Ana Marisa
Año de publicación
2022
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The COVID-19 pandemic, caused by SARS-CoV-2, had its first cases identified in late 2019 and was considered a clinical pandemic in March 2020. In March 2022, more than 500 million people were infected and 6,2 million died as a result of this disease, increasingly associated with changes in human hemostasis, such as hypercoagulation. Numerous factors contribute to the hypercoagulable state, and endothelial dysfunction is the main one, since the activation of these cells can strongly activate platelets and the coagulation system. In addition, there is a dysregulation of the renin-angiotensin system due to the SARS-CoV-2 takeover of the angiotensin converting enzyme 2, resulting in a strong immune response that could further damage the endothelium. Thrombus formation in the pulmonary microvasculature structure in patients with COVID-19 is an important factor to determine the severity of the clinical picture and the outcome of this disease. This review describes the hemostatic changes that occur in SARS-CoV-2 infection, to further improve our understanding of pathogenic mechanisms and the interaction between endothelium dysfunction, kallikrein-kinins, renin angiotensin, and the Coagulation/fibrinolysis systems as underlying COVID-19 effectors. This knowledge is crucial for the development of new effective therapeutic approaches, attenuating the severity of SARS-CoV-2’s infection and to reduce the deaths.
Fil: Aparecida de Andrade, Sonia Aparecida. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: de Souza, Daniel Alexandre. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: Torres, Amarylis Lins. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: Ferreira Graça de Lima, Cristiane. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: Ebram, Matteo Celano. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: Celano Ebram, Rosa Maria. Universidade de Taubate; Brasil
Fil: Schattner, Mirta Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Chudzinski Tavassi, Ana Marisa. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Materia
COAGULOPATHY
COVID-19
HEMOSTASIS
SARS-COV-2
THROMBUS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/210658
Acceder
id CONICETDig_1bfca6ddb67aa9ecd5021ebf97d5aefe
oai_identifier_str oai:ri.conicet.gov.ar:11336/210658
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Pathophysiology of COVID-19: Critical Role of HemostasisAparecida de Andrade, Sonia Aparecidade Souza, Daniel AlexandreTorres, Amarylis LinsFerreira Graça de Lima, CristianeEbram, Matteo CelanoCelano Ebram, Rosa MariaSchattner, Mirta AnaChudzinski Tavassi, Ana MarisaCOAGULOPATHYCOVID-19HEMOSTASISSARS-COV-2THROMBUShttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3The COVID-19 pandemic, caused by SARS-CoV-2, had its first cases identified in late 2019 and was considered a clinical pandemic in March 2020. In March 2022, more than 500 million people were infected and 6,2 million died as a result of this disease, increasingly associated with changes in human hemostasis, such as hypercoagulation. Numerous factors contribute to the hypercoagulable state, and endothelial dysfunction is the main one, since the activation of these cells can strongly activate platelets and the coagulation system. In addition, there is a dysregulation of the renin-angiotensin system due to the SARS-CoV-2 takeover of the angiotensin converting enzyme 2, resulting in a strong immune response that could further damage the endothelium. Thrombus formation in the pulmonary microvasculature structure in patients with COVID-19 is an important factor to determine the severity of the clinical picture and the outcome of this disease. This review describes the hemostatic changes that occur in SARS-CoV-2 infection, to further improve our understanding of pathogenic mechanisms and the interaction between endothelium dysfunction, kallikrein-kinins, renin angiotensin, and the Coagulation/fibrinolysis systems as underlying COVID-19 effectors. This knowledge is crucial for the development of new effective therapeutic approaches, attenuating the severity of SARS-CoV-2’s infection and to reduce the deaths.Fil: Aparecida de Andrade, Sonia Aparecida. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; BrasilFil: de Souza, Daniel Alexandre. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; BrasilFil: Torres, Amarylis Lins. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; BrasilFil: Ferreira Graça de Lima, Cristiane. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; BrasilFil: Ebram, Matteo Celano. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; BrasilFil: Celano Ebram, Rosa Maria. Universidade de Taubate; BrasilFil: Schattner, Mirta Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Chudzinski Tavassi, Ana Marisa. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; BrasilFrontiers Media2022-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/210658Aparecida de Andrade, Sonia Aparecida; de Souza, Daniel Alexandre; Torres, Amarylis Lins; Ferreira Graça de Lima, Cristiane; Ebram, Matteo Celano; et al.; Pathophysiology of COVID-19: Critical Role of Hemostasis; Frontiers Media; Frontiers in Cellular and Infection Microbiology; 12; 6-2022; 1-92235-2988CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.3389/fcimb.2022.896972info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:35:04Zoai:ri.conicet.gov.ar:11336/210658instacron: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:34982025-10-22 11:35:04.679CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Pathophysiology of COVID-19: Critical Role of Hemostasis
title Pathophysiology of COVID-19: Critical Role of Hemostasis
spellingShingle Pathophysiology of COVID-19: Critical Role of Hemostasis
Aparecida de Andrade, Sonia Aparecida
COAGULOPATHY
COVID-19
HEMOSTASIS
SARS-COV-2
THROMBUS
title_short Pathophysiology of COVID-19: Critical Role of Hemostasis
title_full Pathophysiology of COVID-19: Critical Role of Hemostasis
title_fullStr Pathophysiology of COVID-19: Critical Role of Hemostasis
title_full_unstemmed Pathophysiology of COVID-19: Critical Role of Hemostasis
title_sort Pathophysiology of COVID-19: Critical Role of Hemostasis
dc.creator.none.fl_str_mv Aparecida de Andrade, Sonia Aparecida
de Souza, Daniel Alexandre
Torres, Amarylis Lins
Ferreira Graça de Lima, Cristiane
Ebram, Matteo Celano
Celano Ebram, Rosa Maria
Schattner, Mirta Ana
Chudzinski Tavassi, Ana Marisa
author Aparecida de Andrade, Sonia Aparecida
author_facet Aparecida de Andrade, Sonia Aparecida
de Souza, Daniel Alexandre
Torres, Amarylis Lins
Ferreira Graça de Lima, Cristiane
Ebram, Matteo Celano
Celano Ebram, Rosa Maria
Schattner, Mirta Ana
Chudzinski Tavassi, Ana Marisa
author_role author
author2 de Souza, Daniel Alexandre
Torres, Amarylis Lins
Ferreira Graça de Lima, Cristiane
Ebram, Matteo Celano
Celano Ebram, Rosa Maria
Schattner, Mirta Ana
Chudzinski Tavassi, Ana Marisa
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv COAGULOPATHY
COVID-19
HEMOSTASIS
SARS-COV-2
THROMBUS
topic COAGULOPATHY
COVID-19
HEMOSTASIS
SARS-COV-2
THROMBUS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The COVID-19 pandemic, caused by SARS-CoV-2, had its first cases identified in late 2019 and was considered a clinical pandemic in March 2020. In March 2022, more than 500 million people were infected and 6,2 million died as a result of this disease, increasingly associated with changes in human hemostasis, such as hypercoagulation. Numerous factors contribute to the hypercoagulable state, and endothelial dysfunction is the main one, since the activation of these cells can strongly activate platelets and the coagulation system. In addition, there is a dysregulation of the renin-angiotensin system due to the SARS-CoV-2 takeover of the angiotensin converting enzyme 2, resulting in a strong immune response that could further damage the endothelium. Thrombus formation in the pulmonary microvasculature structure in patients with COVID-19 is an important factor to determine the severity of the clinical picture and the outcome of this disease. This review describes the hemostatic changes that occur in SARS-CoV-2 infection, to further improve our understanding of pathogenic mechanisms and the interaction between endothelium dysfunction, kallikrein-kinins, renin angiotensin, and the Coagulation/fibrinolysis systems as underlying COVID-19 effectors. This knowledge is crucial for the development of new effective therapeutic approaches, attenuating the severity of SARS-CoV-2’s infection and to reduce the deaths.
Fil: Aparecida de Andrade, Sonia Aparecida. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: de Souza, Daniel Alexandre. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: Torres, Amarylis Lins. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: Ferreira Graça de Lima, Cristiane. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: Ebram, Matteo Celano. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
Fil: Celano Ebram, Rosa Maria. Universidade de Taubate; Brasil
Fil: Schattner, Mirta Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Chudzinski Tavassi, Ana Marisa. Governo do Estado de Sao Paulo. Secretaria da Saude. Instituto Butantan; Brasil
description The COVID-19 pandemic, caused by SARS-CoV-2, had its first cases identified in late 2019 and was considered a clinical pandemic in March 2020. In March 2022, more than 500 million people were infected and 6,2 million died as a result of this disease, increasingly associated with changes in human hemostasis, such as hypercoagulation. Numerous factors contribute to the hypercoagulable state, and endothelial dysfunction is the main one, since the activation of these cells can strongly activate platelets and the coagulation system. In addition, there is a dysregulation of the renin-angiotensin system due to the SARS-CoV-2 takeover of the angiotensin converting enzyme 2, resulting in a strong immune response that could further damage the endothelium. Thrombus formation in the pulmonary microvasculature structure in patients with COVID-19 is an important factor to determine the severity of the clinical picture and the outcome of this disease. This review describes the hemostatic changes that occur in SARS-CoV-2 infection, to further improve our understanding of pathogenic mechanisms and the interaction between endothelium dysfunction, kallikrein-kinins, renin angiotensin, and the Coagulation/fibrinolysis systems as underlying COVID-19 effectors. This knowledge is crucial for the development of new effective therapeutic approaches, attenuating the severity of SARS-CoV-2’s infection and to reduce the deaths.
publishDate 2022
dc.date.none.fl_str_mv 2022-06
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/11336/210658
Aparecida de Andrade, Sonia Aparecida; de Souza, Daniel Alexandre; Torres, Amarylis Lins; Ferreira Graça de Lima, Cristiane; Ebram, Matteo Celano; et al.; Pathophysiology of COVID-19: Critical Role of Hemostasis; Frontiers Media; Frontiers in Cellular and Infection Microbiology; 12; 6-2022; 1-9
2235-2988
CONICET Digital
CONICET
url http://hdl.handle.net/11336/210658
identifier_str_mv Aparecida de Andrade, Sonia Aparecida; de Souza, Daniel Alexandre; Torres, Amarylis Lins; Ferreira Graça de Lima, Cristiane; Ebram, Matteo Celano; et al.; Pathophysiology of COVID-19: Critical Role of Hemostasis; Frontiers Media; Frontiers in Cellular and Infection Microbiology; 12; 6-2022; 1-9
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/doi/10.3389/fcimb.2022.896972
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Frontiers Media
publisher.none.fl_str_mv Frontiers Media
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
_version_ 1846781981589766144
score 12.982451

Publicaciones similares