PANX1 and triple-A syndrome: The role of aortic endothelial cells (ECs) and its crosstalk with immune cells (macrophages) and SMCs was recently described as we demonstrated that EC-dependent pannexin-1 (Panx 1) channels supports the flux of signaling mediators like ATP that modulate aortic inflammation and vascular remodeling via activation of purinergic signaling resulting in AAA formation (13).