(i) illustrates that the deposition of lipids and macrophages on the vascular wall can lead to abnormal NO secretion mediated by eNOS in endothelial cells and exacerbate iNOS-mediated pro-inflammatory responses in macrophages, which in turn feedback promotes the formation of vascular plaques. (ii) illustrates that CeO2NPs derived NO by the NOS-like activity can prevent vascular plaque formation via improving endothelial cell function and macrophage function. CeO2NPs simulates the activity of NOS to elevate NO level in serum. This exogenous way to supplement endogenous NO levels continuously can change the re-distribution of blood lipids as well as cell function by altering blood flow status including blood flow shear force