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letter
. 2020 May 21;216:108468. doi: 10.1016/j.clim.2020.108468

Fig. 1.

Fig. 1

Ticagrelor use to prevent sepsis-induced coagulopathy in COVID-19.

(1) SARS-CoV-2 entry into lungs through respiratory droplets.

(2) SARS-CoV-2 binds to ACE2 and enters into alveolar (type II) epithelial cell; SARS-CoV-2 replication into alveolar (type II) epithelial cell; Increased inflammation; Increased vascular remodelling; Endothelial dysfunction; Cardiopulmonary dysfunction.

(3) Pulmonary arteriole.

(4) SARS-CoV-2 binds to ACE2 and enters into endothelial cells; Decreased ACE2; Increased Angiotensin 2; Decreased Angiotensin 1-7; Increased ROS (Reactive Oxygen Species) ; Decreased endothelial NO (Nitric Oxide); Increased endothelial dysfunction; Vascular leakage.

(5) Arteriole and blood cells.

(6) Thrombus formation in dysfunctional and leaky arteriole; Platelet activation promotes thrombosis; PNA (Platelets-neutrophils aggregates) formation; Ticagrelor inhibits thrombus formation.

(7) Platelet activation by ADP binding P2Y12 receptor; PNA (Platelet-Neutrophil Aggregates) formation; NET release by neutrophil; NET contribute to triggering cytokine and ROS release by neutrophil and can alter endothelial barrier, and enhance leakage; Ticagrelor inhibits reversibly P2Y12 receptor and the whole cascade of events described below.