Figure 1.

Disulfiram treatment attenuates the formation and progression of experimental AAAs. Experimental AAAs were induced in ApoE deficient male mice by subcutaneously infusing angiotensin II for 28 days. Mice were treated with gasdermin D inhibitor disulfiram or vehicle (saline) and monitored for AAA formation and progression via ultrasonography. (A): Representative ultrasound images of suprarenal aortas at the baseline and day 28 in vehicle and disulfiram treatment groups following angiotensin II infusion. (B): Mean ± standard deviation of maximal suprarenal aortic diameters at different time points in vehicle- and disulfiram-treated, angiotensin II-infused ApoE deficient mice. Two-way ANOVA followed by two group comparison, 0.05 < ^# p <0.1 and ** p < 0.01 compared to vehicle treatment at same time point. (C): AAA incidence. AAA: the presence of aortic dissection imaged by ultrasonography, a 50% or more increase in aortic diameter over the baseline, or death due to AAA rupture. Log-rank test, ** p < 0.01 compared to vehicle treatment. (D): Mortality due to AAA rupture. n = 13 mice/group. Aortic diameters in panel A: 1.01 mm and 1.61 mm on days 0 and 28 for vehicle treatment and 1.03 mm and 1.29 mm on days 0 and 28 for disulfiram treatment.