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. 2019 Dec 18;10:2919. doi: 10.3389/fimmu.2019.02919

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Copyright © 2019 Xu, Liang, Lin and Yu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential role and mechanism of PKM2 in RA. PKM2 can optimize the supply of energy and synthetic substrates for proliferative synoviocytes and activated immune cells via its glycolytic regulation function. The dimer form of PKM2 can interact with important RA transcription factors, such as STAT3, Bcl-2, HIF-1, and Erk1/2, so as to further regulate cell proliferation, apoptosis, angiogenesis, and immune activation. The local acidic microenvironment caused by increased glycolysis is favorable for synoviocyte invasion, MMP-1 activation, and angiogenesis. p, phosphorylation; Ac, acetylation; FA, fatty acid; AA, amino acid; Nuc, nucleotide; ECM, extracellular matrix.