“…[ 50 ] Through the production of mediators such as tissue plasminogen activator, prostacyclin, NO, and antithrombin III, ECs serve as the guardians of vascular homeostasis, as they prevent blood clotting, platelet activation, and leukocyte adherence and infiltration. [ 51 ] The equilibrium between vasodilation and vasoconstriction is disturbed when ECs are damaged, resulting in events that can worsen AS. When considering activated ECs in atheromatous plaques, available active targets may include expressed adhesion molecules such as E‐selectins, vascular cell adhesion molecule 1 (VCAM‐1), and intercellular adhesion molecule 1 (ICAM‐1).…”