The notion was supported by the data collected from IL-1β-stimulated HAECs (Figure S6C), which illustrated a switch to anaerobic glycolysis, downregulation of mitochondrial biogenesis and metabolism, increased inflammation, ROS production, and hypertension signaling, highlighting suppression of SIRT1, PGC1α, and NRF2 as mediators of these events (Figure 3I). This evidence concerns the gene NFE2L2 and Hypertension.