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Figure 2. The regulatory mechanism of estrogen on macrophages in atherosclerosis. We have elucidated the mechanisms by which estrogen regulates macrophage function in atherosclerosis. Estrogen influences macrophage function through its effects on lipid metabolism, inflammatory responses, and cellular polarization. The specific mechanism of action is as follows: Estrogen promotes cholesterol efflux from macrophages, thereby reducing foam cell formation and delaying the progression of atherosclerosis; estrogen inhibits NF-κB activation, reducing production of pro-inflammatory cytokines TNF-α, IL-1, and IL-6; and estrogen induces metabolic reprogramming in macrophages (enhancing mitochondrial respiration while decreasing reactive oxygen species production), thereby promoting their conversion to anti-inflammatory M2 macrophages. IL-1β: Interleukin-1β; IL-6: interleukin-6; TNF-α: tumor necrosis factor-α; oxLDL: oxidized low-density lipoprotein; ABCA1: ATP-binding cassette transporter A1; ABCG1: ATP-binding cassette transporter G1; SR-A: scavenger receptor A; LOX-1: lectin-like oxidized low-density lipoprotein receptor 1; ROS: reactive oxygen species; OXPHOS: oxidative phosphorylation; Sirt3: sirtuin 3; NF-κB: nuclear factor kappa B. The figure was created with https://app.biorender.com/illustrations/68b8e4b10db6ea9d6bb9adb4.