Fig. 2: GMRSP overexpression represses thoracic aortic dissection formation.

A Male mice were induced with tamoxifen for 5 days at two weeks. One week after the last tamoxifen treatment, GMRSP^OE-flox and SM22α⁺GMRSP^OE-flox mice were treated with 0.25% BAPN monofumarate for four weeks (n = 10 biological replicates per group). B Representative images of the aorta of the mice are shown. C The survival rate was estimated by the Kaplan-Meier method and compared using the Breslow test (n = 10 biological replicates per group). D The incidence of AD was statistically analyzed. E The maximum aortic diameter was measured (n = 10 biological replicates per group). F Representative macroscopic images of aorta sections stained with H&E and EVG, Scale bar: 200 μm and 50 μm. The wall thickness (G) and elastin integrity (H) of each groups were analyzed (n = 10 biological replicates per group). I Immunofluorescence staining of α-SMA (green) and GMRSP (red) in the aorta of the mice is shown. Nuclei were counterstained with DAPI. J Immunofluorescence staining of SM22α (green) and MMP2 (red) in the aorta of the mice is shown. Nuclei were counterstained with DAPI,Scale bar: 200 μm. Data are presented as the mean ± SD.The p values were calculated by a two-tailed unpaired Student’s t-test in (E,G,H). The p values were calculated by Kaplan–Meier analysis and two-sided Breslow Test (C).The data presented in (F,I, J) are representative of three independent experiments. Source data are provided as a Source Data file. GMRSP; glucose metabolism regulatory small protein; SMC; smooth muscle cell; AD, aortic dissection; BAPN, β-aminopropionitrile; H&E, hematoxylin and eosin; EVG, elastic–Van Gieson; SMA, smooth muscle actin; DAPI, 4’,6-diamidino-2-phenylindole; SM22α, smooth muscle protein 22-alpha; MMP2, matrix mettaloproteinase2.