RT Journal Article SR Electronic T1 Potential role of endothelial cell surface ectopic redox complexes in COVID-19 disease pathogenesis JF Clinical Medicine JO Clin Med FD Royal College of Physicians SP clinmed.2020-0252 DO 10.7861/clinmed.2020-0252 A1 Isabella Panfoli YR 2020 UL http://www.rcpjournals.org/content/early/2020/06/28/clinmed.2020-0252.abstract AB The novel coronavirus infectious disease (COVID-19) has rapidly spread and poses a great challenge to researchers, both in elucidating its pathogenic mechanism and developing effective treatments. It has been recently proposed that COVID-19 is an endothelial disease. Indeed, the COVID-19 virus binds to angiotensin-converting enzyme type 2 (ACE2), which is expressed in endothelial cells. ACE2 could be implicated in the production of reactive oxygen species (ROS) caused by endothelial dysfunction due to viral damage. Consequently, oxidative stress could prime these cells to acquire a pro-thrombotic and pro-inflammatory phenotype, predisposing patients to thromboembolic and vasculitic events and to disseminated intravascular coagulopathy (DIC). This implies a pivotal role played by oxygen in the pathogenetic mechanism of COVID-19 disease, in that its availability would tune the oxidant state and consequent damage.