Abstract
The global propagation of SARS-CoV-2 leads to an unprecedented public health emergency. Despite that the lungs are the primary organ targeted by COVID-19, systemic endothelial inflammation and dysfunction is observed particularly in patients with severe COVID-19, manifested by elevated endothelial injury markers, endotheliitis, and coagulopathy. Here, we review the clinical characteristics of COVID-19 associated endothelial dysfunction; and the likely pathological mechanisms underlying the disease including direct cell entry or indirect immune overreactions after SARS-CoV-2 infection. In addition, we discuss potential biomarkers that might indicate the disease severity, particularly related to the abnormal development of thrombosis that is a fatal vascular complication of severe COVID-19. Furthermore, we summarize clinical trials targeting the direct and indirect pathological pathways after SARS-CoV-2 infection to prevent or inhibit the virus induced endothelial disorders.
Keywords: COVID-19; SARS-CoV-2; endothelial dysfunction; immunity; thrombosis.
【저자키워드】 COVID-19, SARS-CoV-2, thrombosis, Immunity, Endothelial dysfunction, breath, 【초록키워드】 Inflammation, clinical trial, thrombosis, severe COVID-19, Clinical characteristics, SARS-COV-2 infection, severity, disease severity, lung, clinical trials, virus, immune, Endothelial dysfunction, Endotheliitis, Coagulopathy, Lungs, Patient, pathway, endothelial injury, public health emergency, Potential biomarker, dysfunction, endothelial, Vascular, disorders, cell entry, potential biomarkers, organ, Prevent, pathological mechanism, addition, inhibit, the disease, elevated, manifested, 【제목키워드】 therapeutic, mechanism, implication,