Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever and a dry cough...

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Autores principales: Yasutomi Higashikuni, Wenhao Liu, Takumi Obana, Masataka Sata
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/59141037c0a5495ebe7b794ba22ab4ca
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spelling oai:doaj.org-article:59141037c0a5495ebe7b794ba22ab4ca2021-11-11T17:28:13ZPathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications10.3390/ijms2221120811422-00671661-6596https://doaj.org/article/59141037c0a5495ebe7b794ba22ab4ca2021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/12081https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever and a dry cough, and spontaneously resolve within ten days. However, in severe cases, COVID-19 leads to atypical bilateral interstitial pneumonia, acute respiratory distress syndrome, and systemic thromboembolism, resulting in multiple organ failure with high mortality and morbidity. SARS-CoV-2 has immune evasion mechanisms, including inhibition of interferon signaling and suppression of T cell and B cell responses. SARS-CoV-2 infection directly and indirectly causes dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction, which interact with each other and are exacerbated by cardiovascular risk factors. In this review, we summarize current knowledge on the pathogenic basis of thromboinflammation and endothelial injury in COVID-19. We highlight the distinct contributions of dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction to the pathogenesis of COVID-19. In addition, we discuss potential therapeutic strategies targeting these mechanisms.Yasutomi HigashikuniWenhao LiuTakumi ObanaMasataka SataMDPI AGarticleCOVID-19endothelial injuryinflammationplatelet activationSARS-CoV-2therapeuticsBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12081, p 12081 (2021)
institution DOAJ
collection DOAJ
language EN
topic COVID-19
endothelial injury
inflammation
platelet activation
SARS-CoV-2
therapeutics
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle COVID-19
endothelial injury
inflammation
platelet activation
SARS-CoV-2
therapeutics
Biology (General)
QH301-705.5
Chemistry
QD1-999
Yasutomi Higashikuni
Wenhao Liu
Takumi Obana
Masataka Sata
Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications
description Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever and a dry cough, and spontaneously resolve within ten days. However, in severe cases, COVID-19 leads to atypical bilateral interstitial pneumonia, acute respiratory distress syndrome, and systemic thromboembolism, resulting in multiple organ failure with high mortality and morbidity. SARS-CoV-2 has immune evasion mechanisms, including inhibition of interferon signaling and suppression of T cell and B cell responses. SARS-CoV-2 infection directly and indirectly causes dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction, which interact with each other and are exacerbated by cardiovascular risk factors. In this review, we summarize current knowledge on the pathogenic basis of thromboinflammation and endothelial injury in COVID-19. We highlight the distinct contributions of dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction to the pathogenesis of COVID-19. In addition, we discuss potential therapeutic strategies targeting these mechanisms.
format article
author Yasutomi Higashikuni
Wenhao Liu
Takumi Obana
Masataka Sata
author_facet Yasutomi Higashikuni
Wenhao Liu
Takumi Obana
Masataka Sata
author_sort Yasutomi Higashikuni
title Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications
title_short Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications
title_full Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications
title_fullStr Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications
title_full_unstemmed Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications
title_sort pathogenic basis of thromboinflammation and endothelial injury in covid-19: current findings and therapeutic implications
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/59141037c0a5495ebe7b794ba22ab4ca
work_keys_str_mv AT yasutomihigashikuni pathogenicbasisofthromboinflammationandendothelialinjuryincovid19currentfindingsandtherapeuticimplications
AT wenhaoliu pathogenicbasisofthromboinflammationandendothelialinjuryincovid19currentfindingsandtherapeuticimplications
AT takumiobana pathogenicbasisofthromboinflammationandendothelialinjuryincovid19currentfindingsandtherapeuticimplications
AT masatakasata pathogenicbasisofthromboinflammationandendothelialinjuryincovid19currentfindingsandtherapeuticimplications
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