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?:abstract
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Emerging evidence has documented that multisystem organ failure in coronavirus disease 2019 (COVID-19) patients is strongly associated with various coagulopathies. Treatments for COVID-19-associated coagulopathy are still a clinical challenge. An advancement in the knowledge of mechanisms of the excessive or inappropriate activation of the complement cascade involved in the genesis of COVID-19-associated coagulopathy might be a fundamental approach for developing novel classes of anticoagulant drugs. In this context, there is emerging evidence indicating that C5a, a component of the complement system, and its receptors (C5aRs) play a critical role in the genesis of the COVID-19-associated hypercoagulable state. Thus, this review describes the mechanisms by which C5a/C5aR signaling participates in the cascade of events involved in the pathophysiology of COVID-19-associated coagulopathy. Furthermore, it highlights the current possibilities for the development of a novel therapeutic approach for COVID-19 patients that targets C5a/C5aRs signaling.
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?:doi
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10.1016/j.cytogfr.2020.12.001
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?:doi
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?:journal
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Cytokine_Growth_Factor_Rev
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?:license
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document_parses/pdf_json/0f02eafde863395f167081f23c8a208b5ba1ef60.json
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document_parses/pmc_json/PMC7733683.xml.json
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?:title
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The roles and potential therapeutic implications of C5a in the pathogenesis of COVID-19-associated coagulopathy
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