The newly arrived macrophages continue the cycle by releasing ROS to convert LDL into ox-LDL, which they then phagocytize and convert into foam cells. This cycle perpetuates until foam cells and SMCs are overloaded and subsequently die. The resultant accumulation of dead foam cells, smooth muscle cells, and dispersed LDL in the intima leads to calcification (calcium ion deposition) at the inflammatory sites. This cascade results in the swelling of the intima, ultimately narrowing the artery due to the hardening of material within the innermost layer of endothelial tissue bordering the blood lumen. A detailed flow diagram depicting the effects of species transport and transformation mechanisms in the etiology of atherosclerosis is presented in Figure . transmigrate through fenestrated endothelial layer. 8) Transmigrated monocytes diffuse into tunica intima and transform into macrophages. 9) oxLDL moves into macrophages and 10) macrophages phagocytose oxLDL. 11) Macrophages transforme into foam cells. 12) Release of inflammatory mediators to attract more monocytes to ECRs. 13) Repeat step 7. 14) Release of more ROS from transmigrated monocytes. 15) Release of inflammatory mediators by the foam cells propels 16) movement of smooth muscle cells (SMC) into intima. 17) Transport of dead foam cells to plaque site. 18) Transport of SMC to plaque site. ) Transport of calcium plaque site. Created with BioRender. Despite significant advancements, several knowledge gaps remain. For instance, the precise biophysical interactions at the molecular level between signaling pathways and mechanical cues in atherosclerosis are not fully understood . Further research into the integrated modeling of chemical transport, reaction kinetics, and biomechanical responses could provide deeper insights and lead to novel therapeutic strategies. The roles of species transport and transformation in the cardiovascular system is pivotal in understanding the pathophysiology of diseases. By integrating chemical transport, reactions, and their coupling with biochemical and biomechanical processes, a clearer picture emerges of how these mechanisms contribute to disease progression and stability. Addressing existing knowledge gaps through interdisciplinary research will enhance our ability to develop more effective interventions for cardiovascular diseases such as atherosclerosis.