Figure 4. Vascular ADAM17 activation results in smooth muscle cell senescence and endothelial inflammation thus changes vascular cell phenotypes leading to AAA,

In VSMCs, ADAM17 activation causes mitochondrial fission via Drp1 which leads to enhanced oxygen consumption and senescence. In EC, TNF-α also stimulates Drp1-dependent mitochondrial fission and subsequent mitochondrial ROS production and NF-κB activation thus sustains EC inflammation. The vascular phenotype changes caused by ADAM17 activation thus contribute to AAA development.