Endothelial dysfunction is recognized as the primary event in atherogenesis, the process leading to the formation of atherosclerotic plaques in the arterial walls. This dysfunction occurs when the endothelial cells that line the blood vessels become impaired due to various risk factors, such as high blood pressure, high cholesterol, smoking, and diabetes.
When endothelial cells are dysfunctional, they lose their normal protective functions, which include maintaining vascular tone and barrier integrity, as well as regulating inflammation and thrombosis. This creates an environment conducive to the infiltration of low-density lipoprotein (LDL) cholesterol and monocytes into the arterial wall. As these lipoproteins accumulate and undergo oxidation, they trigger an inflammatory response, leading to further recruitment of immune cells.
Foam cell formation is a critical step that follows endothelial dysfunction, as oxidized LDL is taken up by macrophages, transforming them into foam cells. While this is part of the atherosclerotic process, it is initiated by the earlier dysfunction of the endothelial layer.
Platelet aggregation and cytokine release are also important in the later stages of atherogenesis, particularly in response to the developed lesions and the inflammation in the vascular system. However, these events occur after endothelial dysfunction sets the stage for atheros