Yinglong Ding

Abstract Thoracic aortic dissection (TAD) is a highly lethal vascular condition closely associated with endothelial cell (EC) dysfunction. γ-Aminobutyric acid (GABA) can be synthesized in ECs and modulate cell functions; however, its underlying roles in TADs are unclear. Untargeted metabolomics revealed that GABA levels are decreased in the aortic intima of TAD patients and that GABA is a hub metabolite involved in TAD pathogenesis.

1 Introduction Thoracic aortic dissection (TAD) is a critical condition that requires immediate surgical intervention.[1] While patients are often asymptomatic before the onset, the disease can progress rapidly, with mortality rates reaching up to 75% within the first 72 h if left untreated.[2] The absence of effective medical therapies for aortic dissection is primarily due to an incomplete understanding of the mechanisms driving disease progression.