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. 2022 Sep 23;9:1017650. doi: 10.3389/fmed.2022.1017650

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Copyright © 2022 Cui, Weiyao, Chenghong, Limei, Xinghua, Bo, Xiaozheng and Haidong.

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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Mitochondrial homeostatic biological processes and the development of RA. This figure depicts the relationship between mitochondrial biogenesis, mitochondrial dynamics, and mitochondrial autophagy and RA. PGC-1 protein is a key protein regulating mitochondrial biogenesis. In RA, PGC-1 mRNA is regulated by METTL3 and YTHDF, which activate the PGC-1α/NRF1/TFAM pathway to inhibit mitochondrial biogenesis and mediate synovial inflammation. Drp1 and DNM1L are key proteins that regulate mitochondrial division, and their aberrant activation in RA binds to the receptors, Mff and Fisl1, and localizes to the outer mitochondrial membrane, mediating mitochondrial fission and the release of inflammatory substances by GTP hydrolase. Disruption of PINK1 and Parkin protein recruitment activates mitochondrial autophagy to inhibit synovial apoptosis and inflammatory factors.