Fibroblast growth factors (FGFs) are versatile peptide growth factors involved in various biological functions, including cell growth, differentiation, embryonic development, angiogenesis, and metabolism. Abnormal FGF/FGF receptor (FGFR) signaling has been linked to multiple diseases such as cancer, metabolic disorders, and inflammatory conditions. Macrophage polarization, which involves distinct functional phenotypes, plays a crucial role in tissue repair, homeostasis, and immune responses. Recent evidence suggests that FGF/FGFR signaling is closely involved in macrophage polarization, making it a potential target for therapeutic manipulation of diseases associated with dysfunctional macrophages. This article provides an overview of the structure, function, and downstream regulatory pathways of FGFs, as well as the crosstalk between FGF signaling and macrophage polarization. It also summarizes the potential applications of modulating FGF signaling to influence macrophage polarization. FGFs have diverse regulatory functions in various physiological processes, including development, tissue repair, metabolism, tissue homeostasis, and cancer development. Macrophages, as key components of the innate immune system, exhibit remarkable plasticity and can adapt to different stimuli, leading to distinct functional phenotypes (M1 and M2). The balance between these phenotypes is crucial for maintaining homeostasis and preventing diseases. FGF signaling plays a significant role in macrophage polarization, with FGFs influencing the expression of FGF components in nearby cells. For example, M1 macrophages enhance the Wnt/β-Catenin signaling pathway, leading to increased FGF18 expression. In contrast, M2 macrophages can upregulate FGF2 and TGF-β expression by secreting IL-10. FGFs also facilitate M1 polarization in conditions like multiple sclerosis and rheumatoid arthritis, while promoting M2 polarization in inflammatory diseases such as chronic obstructive pulmonary disease (COPD) and acute lung injury (ALI). The article highlights the importance of understanding the relationship between FGF signaling and macrophage polarization for developing new therapeutic strategies. FGFs can modulate macrophage polarization through various mechanisms, including the activation of specific signaling pathways and the induction of specific cytokines. This knowledge can be leveraged to target FGF signaling as a potential therapeutic approach for diseases associated with dysregulated macrophage function.Fibroblast growth factors (FGFs) are versatile peptide growth factors involved in various biological functions, including cell growth, differentiation, embryonic development, angiogenesis, and metabolism. Abnormal FGF/FGF receptor (FGFR) signaling has been linked to multiple diseases such as cancer, metabolic disorders, and inflammatory conditions. Macrophage polarization, which involves distinct functional phenotypes, plays a crucial role in tissue repair, homeostasis, and immune responses. Recent evidence suggests that FGF/FGFR signaling is closely involved in macrophage polarization, making it a potential target for therapeutic manipulation of diseases associated with dysfunctional macrophages. This article provides an overview of the structure, function, and downstream regulatory pathways of FGFs, as well as the crosstalk between FGF signaling and macrophage polarization. It also summarizes the potential applications of modulating FGF signaling to influence macrophage polarization. FGFs have diverse regulatory functions in various physiological processes, including development, tissue repair, metabolism, tissue homeostasis, and cancer development. Macrophages, as key components of the innate immune system, exhibit remarkable plasticity and can adapt to different stimuli, leading to distinct functional phenotypes (M1 and M2). The balance between these phenotypes is crucial for maintaining homeostasis and preventing diseases. FGF signaling plays a significant role in macrophage polarization, with FGFs influencing the expression of FGF components in nearby cells. For example, M1 macrophages enhance the Wnt/β-Catenin signaling pathway, leading to increased FGF18 expression. In contrast, M2 macrophages can upregulate FGF2 and TGF-β expression by secreting IL-10. FGFs also facilitate M1 polarization in conditions like multiple sclerosis and rheumatoid arthritis, while promoting M2 polarization in inflammatory diseases such as chronic obstructive pulmonary disease (COPD) and acute lung injury (ALI). The article highlights the importance of understanding the relationship between FGF signaling and macrophage polarization for developing new therapeutic strategies. FGFs can modulate macrophage polarization through various mechanisms, including the activation of specific signaling pathways and the induction of specific cytokines. This knowledge can be leveraged to target FGF signaling as a potential therapeutic approach for diseases associated with dysregulated macrophage function.