HIF1A and atherosclerosis: EC HIF1α activity also promotes the recruitment of atherogenic monocytes (depending on the availability of miR-19a) (Akhtar et al., 2015), and Krüppel−like factor 2 (KLF2), which suppresses glycolytic flux in normal ECs by downregulating PFKFB3, is itself downregulated during atherosclerosis, which may partially explain why hypoxia increases glucose uptake in atherosclerotic plaques, especially in macrophage-rich areas (Folco et al., 2011).