ACE2 and endothelial dysfunction: On the contrary, reduced levels or bioavailability of their physiological counterparts, such as angiotensin-(1–7), which is formed by a main receptor for SARS-CoV-2 (i.e., angiotensin converting enzyme 2; ACE2), prostacyclin, and nitric oxide (NO), can also contribute to the endothelial dysfunction and the hypercoagulation state [32, 34, 35].