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. 2022 Sep 20;10:60. doi: 10.1038/s41413-022-00226-9

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — The NGF, CGRP, CCL2/CCR2, and TNFα signaling pathways in OA-associated pain. NGF acts on its receptor TrkA and mediates pain transmission. CGRP is released from C-fiber terminals and binds with calcitonin receptor-like receptor (CLR) and receptor activity-modifying protein 1 (RAMP1) on adjacent Aδ nerve fibers. High expression of chemokines, such as CCL2 and CX3CL1, and other immune mediators, such as colony-stimulating factor 1 (CSF-1) and CGRP, was detected in the DRG and dorsal horn of the spinal cord