AGT and triple-A syndrome: Many mechanisms have been proposed for AAA formation, and basic research has helped to determine the molecular basis and mediators of aortic damage including angiotensin II, leukotriene-LT4, prostaglandin E2 (PGE2), interleukins, tumor necrosis factor, tissue plasminogen activator, c-Jun N-terminal kinase, NF-κB, rho kinases, osteoprotegerin, chymases, hypoxia-inducible factor-1 (HIF-1), metabolism, SMAD, TGF-β, and its signaling pathway [23, 76, 77].