Endothelial Dysfunction, Inflammation, and Oxidative Stress in COVID-19—Mechanisms and Therapeutic Targets

Figure 2

SARS-CoV-2 enters the human body by binding to ACE2. Activation of RAAS produced a cytokine storm, resulting in the secretion of proinflammatory cytokines/chemokines such as interleukins (ILs), interferon-gamma (IFN-γ), monocyte chemoattractant protein-1 (MCP1), and tumor necrosis factor-alpha (TNF-α). This storm produces a pleiades of phenomena which is associated with preexistent comorbidities that lead to an increase in disease severity (adapted after [31]).