EPO and triple-A syndrome: SIRT1 plays a vital role in metabolism and lifespan improvement,[27] and previous studies have reported that SIRT1 prevents stress‐associated vascular remodeling, vascular stiffness and dissection, and atherosclerosis in mice, indicating the importance of SIRT1 for vascular health.[4] The inhibitory effect of SIRT1 in VSMCs has been confirmed in AngII‐ and CaCl2‐induced AAA models.[4] In this study, we demonstrated that EPO treatment downregulated whereas medium‐dose formoterol treatment upregulated SIRT1 expression in vivo and in vitro.