Mechanism of Atherosclerosis Formation: Why LDL in Blood Lipids is a Key Driver

It is important to understand the causes of atherosclerosis: Research shows that tens of thousands of lipoprotein receptors exist in the body's surrounding tissues, including arterial walls and cell surfaces. These receptors specifically accept certain lipoproteins into the cells for metabolism. The resulting cholesterol is stored within the cells as a raw material for cellular synthesis. When cholesterol storage is excessive, lipoprotein receptors automatically reject external lipoproteins to maintain metabolic balance. Congenital defects or acquired dietary imbalances can increase blood lipoprotein levels. With age, the function of arterial wall cells gradually declines and deteriorates, leading to fat deposition and cell rupture, resulting in atherosclerotic plaques. In the formation of atherosclerosis, different types of lipoproteins play different roles. Chylomicrons (CM) primarily transport exogenous triglycerides. Because chylomicrons are relatively large, they generally cannot enter the arterial wall and therefore have little impact on atherosclerosis. Very low-density lipoprotein (VLDL) primarily transports endogenous triglycerides synthesized in the liver. Because VLDL carries relatively little cholesterol and has relatively large particles, it does not easily pass through the arterial intima. Therefore, normal very low-density lipoprotein (VLDL) generally does not contribute to atherosclerosis. However, the situation is concerning because VLDL consists of 50%–70% triglycerides and 8%–12% cholesterol. Therefore, elevated VLDL levels will lead to increased cholesterol levels in the blood plasma, in addition to elevated triglycerides.

Each type of lipoprotein in the body carries a certain amount of cholesterol, with low-density lipoprotein (LDL) carrying the most. Most LDL in the body is eliminated through liver metabolism, but a small portion can bind to macrophages and form "foam cells." Foam cells have a strong ability to disperse, allowing LDL to easily enter arterial walls and carry cholesterol. Therefore, elevated LDL levels are a warning sign of atherosclerosis. Furthermore, the structural protein of VLDL is apolipoprotein B, which participates in the binding of LDL to atherosclerotic plaques. Therefore, the level of apolipoprotein B in the blood is directly proportional to the incidence of coronary heart disease.