Abstract: Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation and cartilage destruction. An imbalance in macrophage polarization is closely related to the occurrence and development of RA, including a central role for M1 macrophages in promoting inflammation and bone destruction in the cytokine network environment of RA. It is a remarkable fact that the abnormal immune-microenvironment in RA patients promotes the metabolic reprogramming of macrophages, which disrupts the dynamic balance of M1/M2 by regulating the polarization of macrophages, leading to a persistent tissue inflammation. Using drugs to inhibit M1 macrophage polarization or induce M2 macrophage polarization is expected to be an ideal strategy for drug development for RA treatment. This review summarizes the effects of metabolic reprogramming of macrophages on polarization phenotype and the metabolism-related signaling pathways in the RA microenvironment, and provides references for the development of RA drugs that can target macrophage metabolism.