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. 2021 Oct 30;26(21):6570. doi: 10.3390/molecules26216570

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The involvement of numerous bioactive substances in the TLR-dependent MAPK signaling cascade in RA. The TLR receptor attracts (MyD) 88 and other related adaptor proteins are activated (ERK1/2, JNK, P38). The MyD88-dependent system controls the expression of pro-inflammatory cytokines and other immune-related genes, signaling through the MAPK pathway, which in turn leads to the activation of the transcription factor AP-1 in RA. ERK: extracellular regulated kinase; IRF: interferon regulatory transcription factor; My D88: myeloid differentiation primary response 88; TLRs: Toll-like receptors; LPSs: lipopolysaccharide receptor; MAPK: mitogen-activated protein kinase; JNK: Jun N-terminal kinases; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; miR: microRNA; AP1: activator protein 1; p38: a MAPK.