These compounds exert interventional effects on CVDs-related mechanisms such as atherosclerosis, myocardial ischemic injury, myocardial hypertrophy, oxidative stress, and inflammatory responses, by regulating a variety of signaling pathways, including NF-κB, PI3K/Akt, Nrf2/HO-1, AMPK, and TLR4/NF-κB. This evidence concerns the gene PRKAA2 and atherosclerosis.