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These conditions can exacerbate the disease, frequently leading to multiple organ failure ( Patients exhibiting mild COVID-19 symptoms, such as fever and cough, often do not require hospitalization unless they experience dyspnea or hypoxemia (oxygen saturation ≤94% or need for oxygenation or ventilatory support), which are indicative of severe disease states ( SARS-CoV-2 may trigger an exacerbated immune response known as a cytokine storm, characterized by a significant rise in pro-inflammatory cytokines, such as interleukin (IL)-1 and IL-6, chemokines, and a T helper (Th) 1 response ( Endothelial damage is closely linked to increased organ failure risks in COVID-19 patients, with studies demonstrating how the virus triggers endothelial cell dysregulation, enhances pro-inflammatory cytokine production, oxidative stress, and expression of adhesion molecules such as ICAM1, VCAM1, and E-selectin ( Excessive activation of the endothelium and platelets, alongside an exacerbated immune response, often results from an unbalanced reaction between the infectious agent and the host, leading to oxidative system activation and contributing to COVID-19’s pathogenesis ( Oxidative stress is a critical factor in COVID-19’s pathogenesis, occurring when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant capacity