Atherosclerosis is a chronic condition that occurs when cholesterol deposits and plaques form inside the arteries. With time, these deposits harden, occlude the arterial lumen, and provoke decreased tissues and clots that block the artery. Molecular and cellular interactions are critical in the pathophysiology of atherosclerosis. When endothelial cells are injured due to increased plasma cholesterol levels, they provoke the expression of adhesion molecules like vascular adhesion molecule-1 (VCAM-1) and selectins. Increased serum low-density lipoprotein contributes to the progress of atherosclerosis. As soon as monocytes reach the subendothelial space, they are converted into foamy macrophages, which results in cholesterol accumulation, lipoprotein deposition, and new vascular modifications.
The nuclear factor kappa B (NF-κB) path may be triggered by the occurring inflammatory process and cause the expression of new dependent genes that encode adhesion molecules and cytokines. Molecules such as PCAM-1, ICAM-1, and VCAM-1 and cytokines such as IL-1, IL-6, and IL-12. The adhesion of monocytes and lymphocytes on the endothelium surface is observed, promoting chemoattractant secretion and migration of chemokine receptors to the endothelium. Finally, vascular smooth muscle cells also contribute to the process of atherosclerosis. If the vessel is damaged, these cells make adjustments, reduce the expression of certain markers, and lead to migration of cells and progression of lesions. In general, endothelium cells, vascular smooth muscle cells, and adhesion molecules are the main participants in the disease process.