fig1

Figure 1. Triggers and endothelial dysfunction. Diverse initiating stimuli, including ischemia-reperfusion injury, plaque rupture, and systemic inflammation (TNF-α, IL-1β), all amplified by hypertension, diabetes, and hyperhomocysteinemia, converge on the coronary microvascular endothelium. This results in oxidative stress (ROS↑/NO↓), upregulation of adhesion molecules (VCAM-1, ICAM-1), TF exposure, and release of HMGB1 as a damage-associated molecular pattern, establishing a prothrombotic and proinflammatory microenvironment. VCAM-1: Vascular cell adhesion molecule-1; ICAM-1: intercellular adhesion molecule-1; TF: tissue factor; HMGB1: high mobility group box 1; TNF-α: tumor necrosis factor-α; IL-1β: interleukin-1β; ROS: reactive oxygen species; NO: nitric oxide.