On the one hand, HIF-1α activation was shown to promote atherosclerosis initiation and progression [40,41] as well as hypoxia-induced renal fibrogenesis [42,43,44] by stimulating epithelial-to-mesenchymal transition [45] and a2(I) collagen expression through interactions with Smad3 [46]. Here, SMAD3 is linked to atherosclerosis.