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. 2020 Nov 25;9:2048004020959574. doi: 10.1177/2048004020959574

Figure 5.

Figure 5.

Overview of netrin-1 effects in the context of normal physiology and atherosclerosis. (a) Endothelial-derived netrin-1 interacts with UNC5b receptors on the monocyte surface, causing chemorepulsion. (b) In atherosclerosis, pro-inflammatory cytokines act on endothelial cells to downregulate expression of endothelial-derived netrin-1, as well as upregulate endothelial cell adhesion molecules, the resultant effect of both being increased monocyte recruitment to the plaque.