Clinical Significance

Low Density Lipoproteins (LDL) play a key role in causing and influencing the progression of atherosclerosis and, in particular, coronary sclerosis. The LDLs are derived from VLDLs (Very Low-Density Lipoproteins) rich in triglycerides by the action of various lipolytic enzymes and are synthesized in the liver.

The elimination of LDL from plasma takes place mainly by liver parenchymal cells via specific LDL receptors. Elevated LDL concentrations in blood and an increase in their residence time coupled with an increase in the biological modification rate results in the destruction of the endothelial function and a higher LDL-cholesterol uptake in the monocyte/macrophage system as well as by smooth muscle cells in vessel walls. The majority of cholesterol stored in atherosclerotic plaques originates from LDL. The LDL cholesterol value is the most powerful clinical predictor among all of the single parameters with respect to coronary atherosclerosis. Therefore, therapies focusing on lipid reduction primarily target the reduction of LDL cholesterol which is then expressed in an improvement of the endothelial function, prevention of atherosclerosis and reducing its progression as well as preventing plaque rupture. 

_{Source: Roche Cobas LDLC3 Method Sheet Version 4.0 2024-09}