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68 reviewsWith the deepening of epigenetic research, studies have shown that N6-methyladenosine (m6A) is closely related to thedevelopment of rheumatoid arthritis (RA), but the mechanism is still unclear. In the study, we collected synovial tissues from normalcontrols and patients with osteoarthritis (OA) or RA. The levels of m6A and inflammation were analyzed by immunofluorescencestaining and western blotting. The roles of IGF2BP3 in cell proliferation and inflammatory activation were explored usingtransfection and RNA immunoprecipitation assays. IGF2BP3−/− mice were generated and used to establish an arthritis mouse modelby transferring serum from adult arthritis K/BxN mice. We found m6A levels were markedly increased in RA patients and mousemodels, and the expression of IGF2BP3 was upregulated in individuals with RA and related to the levels of inflammatory markers.IGF2BP3 played an important part in RA-fibroblast-like synoviocytes (FLS) by promoting cell proliferation, migration, invasion,inflammatory cytokine release and inhibiting autophagy. In addition, IGF2BP3 inhibited autophagy to reduce ROS production,1234567890();,:thereby decreasing the inflammatory activation of macrophages. More importantly, RASGRF1-mediated mTORC1 activation playeda crucial role in the ability of IGF2BP3 to promote cell proliferation and inflammatory activation. In an arthritis model of IGF2BP3−/−mice, IGF2BP3 knockout inhibited RA-FLS proliferation and inflammatory infiltration, and further ameliorated RA joint injury. Ourstudy revealed an important role for IGF2BP3 in RA progression. The targeted inhibition of IGF2BP3 reduced cell proliferation andinflammatory activation and limited RA development, providing a potential strategy for RA therapy.
