“…In addition to genetic mutations, phenotypic transformation of vascular smooth muscle cells (VSMCs) [ 5 ], dysfunction of endothelial cells [ 6 ], infiltration of immune cells [ 7 ], and abnormal interactions between vascular cells [ 8 ] have been reported to contribute to the pathological remodeling of the aorta, ultimately leading to TAD. Aortic extracellular matrix (ECM) degradation and medial degeneration are key histopathologic features of TAD, yet the detailed mechanisms remain incompletely understood, which significantly hampers progress in drug development [ 9 ]. Therefore, elucidating the pathogenesis of TAD and developing effective conservative treatments are urgent priorities.…”