ApoB

Apolipoprotein B (apoB) represents the total concentration of atherogenic lipoprotein particles in the circulation and more accurately reflects the atherogenic burden of lipoproteins than does low-density lipoprotein cholesterol (LDL-C). ^[1] Because each very-low-density lipoprotein, intermediate-density lipoprotein, low-density lipoprotein and lipoprotein(a) particle carries exactly one apoB molecule, the apoB concentration is a direct count of the number of atherogenic particles. ^{[2] [3]} Apolipoprotein B-100 is the major structural component of VLDL, IDL, LDL and lipoprotein(a), while apolipoprotein B-48 is a truncated isoform that forms the backbone of chylomicrons. ^[3]

Atherosclerosis is driven by the trapping of LDL and other apoB-containing lipoproteins within the artery wall, where retained particles accumulate over time and increase plaque burden. ^{[4] [5]} Cholesterol can only enter the arterial wall within apoB particles, so the mass of cholesterol deposited is determined by the number of apoB particles trapped in the wall rather than by the cholesterol content of any single particle. ^[2] In the artery wall LDL is retained in the subendothelial space by binding to proteoglycans via specific sites on apoB, triggering particle modification, foam-cell formation and the inflammatory response that builds the necrotic plaque core. ^[5] Because the atherogenic effect depends on both the magnitude and the duration of exposure, maintaining low apoB-containing particle levels over time slows plaque progression and substantially reduces the lifetime risk of atherosclerotic cardiovascular disease. ^[4]