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. 2022 Nov 8;72(1):117–132. doi: 10.1007/s00011-022-01663-2

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 9 — Schematic summarizing the mechanism by which STING promotes BCP. The expression level of STING in the DRG was significantly increased in BCP rats, sequentially activating the TBK1/IKK/NF-κB/proinflammatory factor axis to promote neuroinflammation and eventually induce enhanced BCP. After intraperitoneal injection of C-176, the level of STING in the BCP rats was decreased, and the TBK1/IKK/NF-κB/proinflammatory factor signaling pathway was then inhibited. Therefore, STING inhibition in the DRG relieved peripheral sensitization, which ultimately alleviated BCP. This figure was drawn with Figdraw (www.figdraw.com) (color figure online)