Abstract
Coronavirus disease 2019 (COVID-19) has infected more than 470 million people and caused more than 6 million deaths worldwide. The high mortality mainly owes to the associated acute respiratory distress syndrome (ARDS), which is characterised by the sudden onset of noncardiogenic pulmonary oedema and hypoxemia.1 Recent studies have revealed that COVID-19 ARDS is a dysregulated host response of inflammation, immunity, and interferon signalling.2 Increasing evidence also suggests that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exerts detrimental effects on the capillary endothelium, possibly by altering the integrity of the endothelial barrier or promoting a pro-coagulant state and the resulted endothelial inflammation.
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