We and others have previously demonstrated that PlGF, MT1, MT2, and CTGF are induced by nonlaminar proatherogenic flow38 and that PlGF, MT1, and MT2 have enhanced Aldo regulation in the aortic arch compared with the descending aorta.26 Thus, we focused on PlGF because it is a secreted growth factor known to promote monocyte chemotaxis.29 Aldo treatment significantly enhanced PlGF protein release from the aortas of ApoE−/− mice (Figure 4B), supporting PlGF as a potential local mediator of Aldo‐induced atherosclerosis. This evidence concerns the gene CCN2 and atherosclerosis.