Figure 2. Retention of apoB-LPs incites monocyte recruitment in early atherosclerotic lesions.

ApoB-LPs enter the intima, bind to proteoglycans, and undergo various modifications, including oxidation and hydrolysis by sPLA₂ and S-SMase. These modifications incite an inflammatory response characterized by chemokine secretion and altered expression of adhesion molecules by the overlying endothelial cells; cause lipoprotein aggregation; and further promote lipoprotein retention. The inflammatory signals lead to monocyte recruitment into the intima, where they differentiate into macrophages and internalize native and modified lipoproteins resulting in foam cell formation. Moreover, foam cells can contribute further to, and thus amplify, lipoprotein modifications and retention (dotted arrow).