Aortic aneurysm and dissection (AAD) are life-threatening conditions characterized by progressive aortic dilation and acute aortic complications. Despite advances in surgical and endovascular management, effective pharmacological strategies to prevent AAD expansion and rupture are still lacking. The pathogenesis of AAD is increasingly understood to be driven by profound cellular heterogeneity within the aortic trilaminar wall, where diverse cell subpopulations contribute differentially to diseas
