Modeling the effects of Cardiomyocyte through Atherosclerosis Progression on Myocardial Infarction

Myocardial infarction, a major cause of cardiovascular disease and death, often arises from atherosclerosis, where the buildup of arterial plaques obstructs blood flow to the heart, ultimately leading to cardiomyocyte death. Being highly sensitive to factors such as oxidized LDL, immune responses, and plaque formation, this condition requires a deeper understanding of the underlying mechanisms. In this study, a comprehensive analysis is conducted to explore the complex biochemical processes driving atherosclerosis, focusing on the interactions between oxidized LDL, monocytes, macrophages, foam cells, and cardiomyocytes. The study shows how the accumulation of oxidized LDL in the arterial walls triggers a cascade of immune responses, including the recruitment of monocytes, their differentiation into macrophages, and the formation of foam cells. These foam cells play a crucial role in the development of atherosclerotic plaques, which further restrict blood flow and accelerate myocardial damage. The findings indicate that an increased intake of oxidized LDL accelerates foam cell formation, intensifying the progression of both atherosclerosis and myocardial infarction. This study emphasizes the pivotal role of oxidized LDL in cardiovascular disease and suggests potential strategies for slowing plaque formation and improving heart health.

• Supervision