Recently we demonstrated that SAA induces macrophage foam cell formation. In this study we show that SAA-induced foam cell formation is inhibited by formyl peptide receptor 2 (FPR2) antagonist WRW4, as well as by FPR2-targeted siRNA knockdown. SAA-stimulated LOX1 expression was also mediated by FPR2. We also found that SAA-stimulated foam cell formation and LOX1 expression was pertussis toxin-insensitive. In addition, FPR2 is upregulated in peripheral blood mononuclear cells from patients with atherosclerosis. Our findings therefore suggest that SAA stimulates foam cell formation via FPR2 signaling and LOX1 induction, and thus likely contributes to atherogenesis. (C) 2013 Elsevier Inc. All rights reserved.