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. 2021 Jun 30;22(3):926. doi: 10.3892/etm.2021.10358

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Copyright: © Hu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Schematic model of m6A in regulating arthritis. (A) METTL3 knockdown decreases chondrocyte apoptosis rate and inflammatory cytokine levels. In addition, METTL3 knockdown promotes degradation of the extracellular matrix by suppressing the expression levels of MMP-13 and Coll X, while elevating the expression levels of Aggrecan and Coll II. (B) METTL3-deficiency-mediated loss of m6A leads to slower SOCS mRNA degradation and increased SOCS protein levels, thereby blocking the IL-7 pathway and eventually disrupting the differentiation and proliferation of naïve T cells. m6A, RNA N6-methyladenine; METTL, methyltransferase-like; MMP, matrix metalloproteinase; Coll, collagen; IL, interleukin.