Gasdermin D deficiency attenuates development of ascending aortic dissections in a novel mouse model
This study established a novel mouse model for TAD. Bulk RNA sequencing was performed to investigate the mechanisms underlying TAD pathogenesis in this model. The data revealed acute inflammation activation in both TAD and control aortas. However, while inflammation in control aortas resolved within two weeks, TADs exhibited a sustained inflammatory response throughout the observation period. Ingenuity Pathway Analysis and functional annotation of differentially expressed genes indicated that a distinct inflammatory microenvironment, rather than generalized inflammation, drives TAD onset by specifically recruiting neutrophils to the aortic wall. At later stages, T-cell-mediated immune injury became the predominant driver of pathology Overall design: TADs and control aortas were collected on days 7 and 14, with ascending aortas from age-matched naïve mice serving as baseline references (n=6 per group). Comparisons were conducted to assess temporal differences (d0 vs d7 vs. d14) and pathology-specific differences (TAD vs. control aorta) in gene expression during TAD development.