COVID-19 associated cardiac disease: Is there a role of neutrophil extracellular traps in pathogenesis?
The COVID-19 pandemic has driven an upheaval of new research, providing key insights into the pathogenesis of this disease. Lymphocytopenia, hyper-inflammation and cardiac involvement are prominent features of the disease and have prognostic value. However, the mechanistic links among these phenomen...
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Published in: | AIMS molecular science Vol. 8; no. 4; pp. 275 - 290 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
AIMS Press
01-12-2021
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Subjects: | |
Online Access: | Get full text |
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Summary: | The COVID-19 pandemic has driven an upheaval of new research, providing key insights into the pathogenesis of this disease. Lymphocytopenia, hyper-inflammation and cardiac involvement are prominent features of the disease and have prognostic value. However, the mechanistic links among these phenomena are not well understood. Likewise, some COVID-19 patients exhibit multi-organ failure with diseases affecting the cardiac system, appearing to be an emerging feature of the COVID-19 pandemic. Neutrophil extracellular traps (NETs) have been frequently correlated with larger infarct sizes and can predict major adverse cardiac events. However, the exact mechanism behind this remains unknown. Although the excessive NET formation can drive inflammation, particularly endothelial and promote thrombosis, it is essential to normal immunity. In this paper, we postulate the role of NETs in cardiac disease by providing an overview of the relationship between NET and inflammasome activities in lung and liver diseases, speculating a link between these entities in cardiac diseases as well. Future research is required to specify the role of NETs in COVID-19, since this carries potential therapeutic significance, as inhibition of NETosis could alleviate symptoms of this disease. Knowledge gained from this could serve to inform the assessment and therapeutics of other hyper inflammatory diseases affecting the heart and vasculature alike. |
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ISSN: | 2372-0301 2372-0301 |
DOI: | 10.3934/molsci.2021021 |