ELN and triple-A syndrome: Similar to human AAA, aortic wall dilation [10], aneurysm rupture [10], adipogenesis in the adventitial wall [11,12,13], the presence of intraluminal thrombus [6,14], vascular wall thickness [15], medial wall thinning with smooth muscle cell (SMC) depletion [16], degradation of collagen and elastin fibers [10], gelatinolytic activity [17,18], oxidative stress due to the increased production of reactive oxygen species (ROS) [19,20], and VV stenosis [7] have been reported in hypoperfusion-induced AAA animal models [8,9,21].