In addition to the effects associated with glucose and lipid metabolism described above, activation of the downstream effects of AMPK are reflected in endothelial cell function enhancement and cardiovascular homeostasis maintenance via increased eNOS activity and nitrous oxide (NO) production via eNOS phosphorylation [28,29]; reduced cardiac hypertrophy via ERK inhibition [30]; activated SIRT1-PGC-1α pathway to promote mitochondrial biogenesis [31,32]; and reduced inflammatory responses via NF-κB/TNF-α pathway inhibition [26]. Here, NFKB1 is linked to cardiac hypertrophy.