Several studies suggest that Wnt1, Wnt2, and Wnt3a mediate a direct link between canonical Wnt signaling and VSMC proliferation in the neointimal formation of atherosclerosis.274 Upregulation of Wnt3a reduced the content of blood lipid, decreased the levels of inflammatory cytokines and oxidative stress, and increased plaque stability in ApoE−/− mice.275 Canonical Wnt signaling and LRP5 are also involved in the formation of macrophage foam cells in humans.276. Here, WNT3A is linked to atherosclerosis.