APOB and atherosclerosis: Although these mechanisms occur without prior endothelial damage, permissive conditions like endothelial dysfunction, inflammation, and structural alterations, such as the absence of a confluent luminal elastin sheet, and exposure of arterial proteoglycans, not only increase ApoB-containing lipoproteins delivery in the intima but also accelerate the subendothelial deposition of lipids and contribute to the onset and progression of atherosclerosis (40, 45, 47, 48).