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. 2023 Sep 18;19(15):4915–4930. doi: 10.7150/ijbs.86039

Figure 4.

Figure 4

Metabolism of TAMs affects M2 conversion. (a) Glucose metabolism. M1 TAMs metabolize through aerobic glycolysis, enhancing the PPP for NADPH. M2 TAMs depend more on oxidative phosphorylation, reducing PPP and NADPH, promoting cancer progression. CARKL regulates PPP; miR-375 and Slit2 from BCCs promote glycolysis in macrophages, increasing the antitumor phenotype. Aberrantly activated HH signaling supports the OXPHOS-promoting M2 phenotype. (b) Amino acid metabolism. BCCs shift from NO to polyamine synthesis in arginine metabolism, affecting TAM activity. Sepiapterin normalizes arginine metabolism, inhibiting cancer progression. Tryptophan metabolite receptors on TAMs enhance antitumor immunity. (c) Iron metabolism. M1 TAMs sequester iron, M2 TAMs release iron. znPPIX repolarizes M2 to M1-type. TAM-derived LCN-2 transports iron to BCCs, promoting pro-breast cancer development. (d) Adenosine metabolism. Increased ADA2 activity in TAMs induces a pro-tumor M2 phenotype. Adenosine from BCCs promotes angiogenesis through A2A receptors and stimulates VEGF production in macrophages. (Sketch created using Biorender.com.)