Figure 7.

Schematic illustration of Mac-1 (macrophage-1 antigen) activation induced by FAM3D (family with sequence similarity 3, member D). Pathological stimuli including TNF-α, LPS, and OSS promote the expression and secretion of endothelial cell (EC)–generated FAM3D. FAM3D activates Mac-1 on neutrophils through FPR (formyl peptide receptor) 1 and FPR2, dependent on Gi-protein- and β-arrestin-related signals. The activated Mac-1 interacts with ICAM-1 on the endothelial surface, mediating neutrophil recruitment and abdominal aortic aneurysm (AAA) development. ICAM-1 indicates intercellular adhesion molecule 1; LPS, lipopolysaccharide; OSS, oscillatory shear stress; and TNF-α, tumor necrosis factor α.