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. 2022 May 19;13:867260. doi: 10.3389/fimmu.2022.867260

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Copyright © 2022 Cutolo, Campitiello, Gotelli and Soldano

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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Intracellular signaling and metabolic pathways activated into RA pro-inflammatory M1 macrophages. Intracellular signaling and metabolic pathways activated in M1 macrophages that contribute to their pro-inflammatory role in the inflammatory process in RA. TLR4, Toll-like receptor 4; IL-6R, interleukine-6 receptor; IL-1βR, interleukine-1β receptor; TNFR, tumor necrosis factor receptor; NFkB, nuclear factor-kB; SAPK: stress-activated protein kinases; MAPK, mitogen-activated protein kinases; JAK, Janus kinase; STAT, signal transducer and activators of transcription; Erk1/2, extracellular signal-regulated protein kinases 1 and 2; JNK, Jun N-terminal kinase; TFs, transcription factors; AKT, protein kinase B; mTOR, mechanistic target of rapamycin; HIF-1α, hypoxia-inducible factor-1α; ROS, reactive oxygen species; /, break in Krebs cycle.