Pathophysiology of COVID-19: critical role of hemostasis

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dc.contributor(BCA) Laboratório de Biofármacospt_BR
dc.contributorIniciação Científicapt_BR
dc.contributorPrograma de Pós-Graduação em Ciências – Toxinologia (PPGTox)pt_BR
dc.contributor(CENTD) Centro de Excelência para Descoberta de Alvos Molecularespt_BR
dc.contributor(LDI) Laboratório de Desenvolvimento e Inovação Industrialpt_BR
dc.contributor.authorChudzinski, Sonia Aparecida de Andradept_BR
dc.contributor.authorSouza, Daniel Alexandre dept_BR
dc.contributor.authorTorres, Amarylis Linspt_BR
dc.contributor.authorLima, Cristiane Ferreira Graça dept_BR
dc.contributor.authorEbram, Matteo Celanopt_BR
dc.contributor.authorCelano, Rosa Maria Gaudiosopt_BR
dc.contributor.authorSchattner, Mirtapt_BR
dc.contributor.authorChudzinski-Tavassi, Ana Marisapt_BR
dc.date.accessioned2022-06-22T15:54:53Z-
dc.date.available2022-06-22T15:54:53Z-
dc.date.issued2022pt_BR
dc.identifier.citationChudzinski SAA, Souza DA, Torres AL, Lima CFG, Ebram MC, Celano RMG, et al. Pathophysiology of COVID-19: critical role of hemostasis. Front. Cell. Infect. Microbiol. 2022 June;12:896972. doi:10.3389/fcimb.2022.896972.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/4400-
dc.description.abstractThe 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.pt_BR
dc.description.sponsorship(CNPq) Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorship(CAPES) Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.description.sponsorship(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.format.extent896972pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofFrontiers in Cellular and Infection Microbiologypt_BR
dc.rightsOpen accesspt_BR
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/pt_BR
dc.titlePathophysiology of COVID-19: critical role of hemostasispt_BR
dc.typeArticlept_BR
dc.rights.licenseCC BYpt_BR
dc.identifier.doi10.3389/fcimb.2022.896972pt_BR
dc.identifier.urlhttps://doi.org/10.3389/fcimb.2022.896972pt_BR
dc.contributor.external(UNITAU) Universidade de Taubatépt_BR
dc.contributor.external(CONICET) Consejo Nacional de Investigaciones Cientificas y Tecnicaspt_BR
dc.contributor.externalAcademia Nacional de Medicina de Buenos Airespt_BR
dc.identifier.citationvolume12pt_BR
dc.subject.keywordCOVID-19pt_BR
dc.subject.keywordSARS-CoV-2pt_BR
dc.subject.keywordhemostasispt_BR
dc.subject.keywordcoagulopathypt_BR
dc.subject.keywordthrombuspt_BR
dc.relation.ispartofabbreviatedFront. Cell. Infect. Microbiolpt_BR
dc.identifier.citationabntv. 12, 896972, jun. 2022pt_BR
dc.identifier.citationvancouver2022 June;12:896972pt_BR
dc.contributor.butantanChudzinski, Sonia Aparecida de Andrade|:Pesquisador:Docente Colaborador PPGTox|:(BCA) Laboratório de Biofármacos|:PrimeiroAutorpt_BR
dc.contributor.butantanSouza, Daniel Alexandre de|:Desvinculado|:(BCA) Laboratório de Biofármacospt_BR
dc.contributor.butantanTorres, Amarylis Lins|:Aluno|:(BCA) Laboratório de Biofármacos:Iniciação Científicapt_BR
dc.contributor.butantanLima, Cristiane Ferreira Graça de|:Aluno|:(BCA) Laboratório de Biofármacos:Programa de Pós-Graduação em Ciências – Toxinologia (PPGTox)pt_BR
dc.contributor.butantanEbram, Matteo Celano|:Aluno|:(BCA) Laboratório de Biofármacos:Iniciação Científicapt_BR
dc.contributor.butantanChudzinski-Tavassi, Ana Marisa|:Pesquisador:Docente Permanente PPGTox|:(CENTD) Centro de Excelência para Descoberta de Alvos Moleculares:(LDI) Laboratório de Desenvolvimento e Inovação Industrial|:Autor de correspondênciapt_BR
dc.sponsorship.butantan(CNPq) Conselho Nacional de Desenvolvimento Científico e Tecnológico¦¦pt_BR
dc.sponsorship.butantan(CAPES) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior¦¦pt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
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