Fig. 3

Genes with abnormal m6A methylation are involved in the pathogenesis of RA. A IGFBP2 influences the interaction between FLS by regulating the neuropeptides GHR and NPR2. IGF2BP3 regulates G2/M transition and affects the polarization of M1 macrophages. SMOC2 controls MYO1C expression through ALKBH5-mediated m6A modification. In RA FLS, these genes promote FLS proliferation through different pathways. B METTL3 promotes FLS activation and inflammation through the NF-κB signaling pathway. METTL3 and YTHDF2 synergically inhibited the expression of PGC-1α and cytochrome C and reduced the ATP production and oxygen consumption rates. C In MH7A cells activated by TNF, the mRNA abundance and m6A methylation abundance of WTAP, RIPK2, JAK3, and TNFRSF10A significantly changed. These genes are involved in the pathogenesis of RA through m6A methylation. D The low expression of ALKBH5, FTO, and YTHDF2 in RA peripheral blood is associated with changes in inflammatory markers and some key pro-inflammatory cytokines. These genes may be biomarkers or predictors for the assessment of RA onset, disease progression, and disease severity