Gout is a metabolic inflammatory disease characterized by acute or chronic inflammatory responses caused by monosodium urate crystal deposition in joints and other tissues, which can eventually lead to osteoarticular damage as the disease progresses. In the early stages of acute gouty inflammation, M1 macrophages secrete pro-inflammatory factors to trigger gouty arthritis. As inflammation progresses, M2 macrophages increase, releasing anti-inflammatory factors to alleviate inflammation. The macrophage polarization is regulated by various metabolic pathways. M1 macrophages mainly rely on glycolysis and the pentose phosphate pathway for ATP, while M2 macrophages depend more on fatty acid oxidation and oxidative phosphorylation. These metabolic shifts influence macrophage phenotypes and functions, either promoting or delaying gout development. Therefore, regulating macrophage polarization and its metabolic activity holds promise as a potential strategy for controlling the inflammation associated with gout. This article will review the impact of macrophage metabolic reprogramming on polarization and changes in related signaling pathways in gout, to provide references for the research and development of gout therapeutic  drugs.

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