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Adipose tissue macrophages are a heterogeneous population of immune cells (macrophages) residing within adipose tissue, comprising a significant fraction of immune cells in both lean and obese states[4]. These cells are derived either from embryonic progenitors or bone marrow, and can be generally characterized as CD68+ or F4/80+ in mouse models[4]. ATMs perform several major functions: they clear dead adipocytes (phagocytosis), produce pro- and anti-inflammatory cytokines, participate in lipid metabolism, present antigens to T cells, regulate tissue remodeling, and support angiogenesis and adipogenesis[3][4][6][7]. Under conditions of obesity, ATMs increase in number, shift toward a pro-inflammatory phenotype (M1-like), and contribute to chronic inflammation, insulin resistance, and metabolic disease[1][3][4][6]. In healthy tissue, ATMs maintain tissue homeostasis and adapt to changing metabolic needs[2][5]. ATMs are being explored as therapeutic targets to mitigate obesity-related metabolic dysfunction, although targeting this cell population presents significant technical and clinical challenges due to their heterogeneity and multifunctionality[3][5][6].
Anti-inflammatory modulation (e.g., GLP-1 analogs reduce ATM-driven inflammation and shift macrophage phenotype); Reduced fat mass and macrophage content through direct and indirect effects on ATMs
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