Several animal studies have indicated that propranolol, a β‐blocker, may be beneficial to AAA because of both hemodynamic properties and biochemical effects on matrix proteins.[44] However, in clinical trials, there was a very small, non‐significant protective effect of propranolol on AAA expansion.[45] In the present study, we discovered the therapeutic effects of formoterol, a β2‐agonist, in EPO‐induced AAA, and gene knockdown of β2AR in VSMCs promoted cellular senescence and inhibited SIRT1 expression. This evidence concerns the gene ADRB2 and triple-A syndrome.