The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in >500,000 deaths worldwide, including >125,000 deaths in the U.S. since its emergence in late December 2019 and June 2020. Neither curative anti-viral drugs nor a protective vaccine is currently available for the treatment and prevention of COVID-19. Recently, new clinical syndromes associated with coagulopathy and vasculopathy have emerged as a cause of sudden death and other serious clinical manifestations in younger patients infected with SARS-CoV-2 infection. Angiotensin converting enzyme 2 (ACE2), the receptor for SARS-CoV-2 and other coronaviruses, is a transmembrane protein expressed by lung alveolar epithelial cells, enterocytes, and vascular endothelial cells, whose physiologic role is to induce the maturation of angiotensin I to generate angiotensin 1-7, a peptide hormone that controls vasoconstriction and blood pressure. In this review, we provide the general context of the molecular and cellular mechanisms of SARS-CoV-2 infection with a focus on endothelial cells, describe the vasculopathy and coagulopathy syndromes in patients with SARS-CoV-2, and outline current understanding of the underlying mechanistic aspects.
【저자키워드】 COVID-19, SARS-CoV-2, ACE2, Inflammatory cytokines, Vasculopathy, vascular inflammation, 【초록키워드】 Treatment, coronavirus disease, Vaccine, coronavirus, SARS-COV-2 infection, Infection, angiotensin converting enzyme, Coagulopathy, endothelial cells, Control, death, epithelial cells, receptor, molecular, anti-viral drug, Protective, Angiotensin 1-7, blood pressure, enterocytes, clinical manifestation, acute respiratory syndrome, maturation, other coronaviruses, syndrome, vascular endothelial cells, vasoconstriction, transmembrane protein, prevention of COVID-19, generate, expressed, induce, cellular mechanism, curative, infected with SARS-CoV-2, lung alveolar, patients with SARS-CoV-2, peptide hormone, younger patient,