Figure 6

A proposed model for the role of SAMB in regulating atherosclerosis. On one hand, SAMB can downregulate the translation and transcription of lipid transporters CD36 and SR-A1, thereby inhibiting the phagocytosis of oxidized low-density lipoprotein by macrophages, reducing foam cell formation and plaque development. On the other hand, SAMB can suppress the expression of inflammatory factors by inhibiting the NF-κB/NLRP3 signaling pathway, resulting in decreased macrophage infiltration in plaques.