Besides inflammation, other pathophysiological mechanisms in relationship with increased OS have been advocated to explain the pathogenesis of COVID-19 [12]: inhibition of angiotensin converting enzyme 2 (ACE-2) activity [13,14,15,16], denaturation of hemoglobin leading to iron metabolism dysregulation with release of toxic free iron ion [17,18,19,20,21], disseminated intravascular coagulation due to hypoxia [12] and endothelial dysfunction [22,23,24,25,26]. Here, ACE2 is linked to endothelial dysfunction.