Schematic diagram depicting endothelial dysfunction (ED) contributing to COVID-19-associated vascular inflammation and coagulopathy. The angiotensin converting enzyme 2 (ACE2) receptor is widely expressed on endothelial cells in the lung, heart, kidney, and intestine, allowing endothelial cells (EC) to be infected by severe acute respiratory syndrome coronarvirus 2 (SARS-CoV-2). The sequence of cellular events leading to ED begins (as early as) immediately for type I EC activation, followed by type II EC activation, EC apoptosis, and EC necrosis. Type I EC activation does not require de novo protein synthesis by means of immediately releasing pro-stored proteins such as von Willebrand factor (vWF), P-selectin, thrombin, and histamine. Conversely, type II EC activation requires de novo protein synthesis by means of releasing new proteins such as vWF, Tissue factor, fibrinogen, E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), interleukin-1 (IL-1), monocyte chemoattractant protein-1, (MCP-1), and C-reactive protein. Endothelial apoptosis results in endothelial detachment by anoikis & denudation of basement membrane, whereas endothelial necrosis results in further release of thrombomudulin and vWF. Finally, leukocyte adhesion molecules, pro-inflammatory cytokines (IL-1, IL-6, and TNF), chemokines (MCP-1), together with pro-coagulant molecules contribute to COVID-19 –associated inflammation and coagulopathy.