A bdominal aortic aneurysm (AAA) is a chronic inflammatory disease characterized by the remodeling of the aortic wall, and it frequently leads to high morbidity and mortality because of vascular dissection and rupture.1 Although AAA formation is a multifactorial process involving the infiltration of macrophages, release of proinflammatory cytokines and proteases, elastin breakdown, vascular smooth muscle cell (VSMC) apoptosis, and increased collagen turnover, macrophages are essential contributors to the pathogenesis of AAAs.2,3 Accordingly, monocytes/macrophages are reportedly activated by chronic inflammatory states, including atherosclerosis and oxidative stress, and by angiotensin II (Ang II) and inflammatory cytokines.Subsequently, macrophages infiltrate vessel walls, release proteases such as elastase, matrix metalloproteinase-12 (MMP-12) and metalloproteinases, and degrade extracellular matrix components such as collagen and elastin. 4,5 Simultaneously, infiltrating macrophages secrete inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interferon-γ, interleukin-1β, and interleukin-6, into the media and adventitia of aneurysmatic vessels, thereby, exacerbating inflammatory responses.
6Macrophage infiltration into vessel walls requires highly coordinated reorganization of actin cytoskeletal structures to create membrane protrusions called podosomes. 7 Human and murine podosomes contain many of the structural components
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