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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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) |
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COVID-19 endothelial injury inflammation platelet activation SARS-CoV-2 therapeutics Biology (General) QH301-705.5 Chemistry QD1-999 |
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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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