CDK5 facilitates the development of endothelial senescence and atherosclerosis by mediating hyperphosphorylation of sirtuin-1, and its knockdown or inhibition decreases the number of senescent endothelial cells and attenuates inflammatory genes expression in porcine aortic endothelial cells [44], but the flavonoids like luteolin can inactivate CDK5 [45]. This evidence concerns the gene CDK5 and atherosclerosis.