Atherosclerosis serves as a prime example of how biochemically enhanced disruptions in biophysical and biomechanical stability via the influence of reactive oxygen species (ROS) lead to severe cardiovascular outcomes. The early stages involve lipid accumulation and foam cell formation, wherein macrophages engulf ox-LDL, exacerbating local inflammation and plaque growth . This progression is inherently linked to the mechanics of blood flow, wall shear stress, and cyclic strain imparted by pulsatile blood pressure, ultimately culminating in plaque rupture or vascular occlusion. The schematic representation in Figure outlines the crucial roles of transport and transformation mechanisms in atherosclerosis pathogenesis. Initially, blood flows through the arterial lumen with high concentrations of glucose (hyperglycemia) and LDL. This dense blood damages endothelial cells, altering their morphology. The damaged endothelial layer becomes fenestrated, allowing LDL to enter the tunica intima and causing the release of ROS from the injured endothelial cells. ROS oxidize LDL, transforming it into ox-LDL, which emits chemical signals that facilitate the adhesion and migration of monocytes from the bloodstream to the endothelial cell receptors. Consequently, monocytes transmigrate into the intima, where they engulf ox-LDL and convert into macrophages. These macrophages, laden with ox-LDL, become foam cells and release inflammatory mediators that attract additional monocytes, stimulate further ROS release, and recruit neutrophils from the bloodstream to the intima. The mediators also stimulate the migration of smooth muscle cells (SMCs) from the media into the intima, where more phagocytosis of ox-LDL occurs.