Functional Characterization of SLC2A3 in Rheumatoid Arthritis: Unraveling Its Role in Ferroptosis and Inflammatory Pathways

ABSTRACT Background Hence, we investigated that the function and effects of SLC2A3 in rheumatoid arthritis (RA) and the underlying mechanism. Methods C57BL/6 mice were immunized with bovine type II collagen to induce mice model of RA. Results The expression of serum SLC2A3 was down‐regulated, and was negative correlation with CRP, RF or anti‐CCP in patients with RA. In mice model of RA, SLC2A3 mRNA and protein expression in joint tissue were reduced. Sh‐SLC2A3 promoted RA and inflammation in mice model. SLC2A3 promoted cell growth and osteogenic differentiation of MC3T3‐E1 cells in vitro model of RA. SLC2A3 reduced ferroptosis in vitro model or mice model of RA. SLC2A3 induced Tiam1 protein expression, and SLC2A3 protein linked with Tiam1 protein in model of RA. Tiam1 reduced the effects of sh‐SLC2A3 on RA and inflammation in mice model. Tiam1 inhibitor the effects of SLC2A3 on osteogenic differentiation and ferroptosis in vitro model of RA. Conclusions Collectively, SLC2A3 reduced inflammation levels and ferroptosis through the inactivation of mitochondrial damage by Tiam1 in model of RA, could serve as a potent therapeutic agent for alleviating RA.