“…Interestingly, ILT correlated positively with wall levels of pro-and active MMP-2, elastase, and plasmin, whereas total wall MMP-9, MMP-2 activation, plasmin activity, and microparticle release correlated with aneurysm diameter. The potential importance of these and other factors in future modeling and therapeutic efforts is highlighted by the attenuation of aneurysmal development in various experimental models of AAA by depletion of neutrophils, T-cells, macrophages, or mast cells [76,90], inhibition of platelet activation [91], inhibition of neutrophil recruitment [92,93], knockout of plasminogen [67], deficiency of uPA [94], knockout of MMP-2, -9, or -12 [95,96], or increases in PAI-1 [97], TIMP-1 [98], or catalase [99].…”