Mouse Low Density Lipoprotein (LDL) ELISA Kit-Sandwich

In mice, the primary function of LDL is as a significant pathogenic factor in atherosclerosis, particularly concerning its impact on macrophages and arterial wall cells following oxidative modification. These effects are not only linked to lipid metabolism and inflammatory responses but also play a crucial role in the pathophysiological development of atherosclerosis. The LDL receptor (LDLR) is a key regulator of LDL metabolism. When LDLR is deficient in mice, it results in increased LDL cholesterol levels in the blood and leads to the development of severe atherosclerotic lesions. LDL is prone to oxidative modification by free radicals, forming oxidized LDL (Ox-LDL). Ox-LDL not only directly promotes the progression of atherosclerosis but also exacerbates lesions by inducing macrophage phagocytosis and the formation of foam cells.