Macrophages are a diverse population of immune cells with functions ranging from homeostasis to immune responses. Their functions depend on both heterogeneity and plasticity, which allows them to adapt to their microenvironment. Macrophages can be categorized into two extremes: pro-inflammatory (M1) and anti-inflammatory/pro-resolving (M2) profiles. M1 macrophages initiate and sustain inflammatory responses by secreting pro-inflammatory cytokines, activating endothelial cells, and recruiting other immune cells. In contrast, M2 macrophages promote inflammation resolution, phagocytose apoptotic cells, drive collagen deposition, and release anti-inflammatory mediators. These phenotypic and functional changes are accompanied by metabolic adaptations. M1 macrophages rely mainly on glycolysis, with two breaks in the TCA cycle leading to the accumulation of itaconate and succinate. Excess succinate stabilizes HIF1α, activating glycolytic genes and sustaining glycolysis. M2 cells, on the other hand, are more dependent on oxidative phosphorylation (OXPHOS), with an intact TCA cycle providing substrates for the electron transport chain (ETC). Both M1 and M2 macrophages exhibit specific metabolic pathways that regulate lipid and amino acid metabolism, affecting their responses. These metabolic adaptations support macrophage activities and their polarization in specific contexts. The review discusses recent findings linking macrophage functions and metabolism, highlighting the dynamic and tissue-specific nature of macrophage polarization.Macrophages are a diverse population of immune cells with functions ranging from homeostasis to immune responses. Their functions depend on both heterogeneity and plasticity, which allows them to adapt to their microenvironment. Macrophages can be categorized into two extremes: pro-inflammatory (M1) and anti-inflammatory/pro-resolving (M2) profiles. M1 macrophages initiate and sustain inflammatory responses by secreting pro-inflammatory cytokines, activating endothelial cells, and recruiting other immune cells. In contrast, M2 macrophages promote inflammation resolution, phagocytose apoptotic cells, drive collagen deposition, and release anti-inflammatory mediators. These phenotypic and functional changes are accompanied by metabolic adaptations. M1 macrophages rely mainly on glycolysis, with two breaks in the TCA cycle leading to the accumulation of itaconate and succinate. Excess succinate stabilizes HIF1α, activating glycolytic genes and sustaining glycolysis. M2 cells, on the other hand, are more dependent on oxidative phosphorylation (OXPHOS), with an intact TCA cycle providing substrates for the electron transport chain (ETC). Both M1 and M2 macrophages exhibit specific metabolic pathways that regulate lipid and amino acid metabolism, affecting their responses. These metabolic adaptations support macrophage activities and their polarization in specific contexts. The review discusses recent findings linking macrophage functions and metabolism, highlighting the dynamic and tissue-specific nature of macrophage polarization.