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. 2020 Feb 8;98(4):527–540. doi: 10.1007/s00109-020-01879-x

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© The Author(s) 2020

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 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. 8 — The mechanisms of RIG-I promoted renal interstitial fibrosis. The expression of RIG-I was induced under pathological stimulation, which activated NF-κB signaling and promoted the synthesis and release of proinflammatory mediators in renal tubular epithelial cells. The proinflammatory cytokines released by renal tubular epithelial cells dramatically enhanced the expression of c-Myc in fibroblasts, which activated TGF-β/Smad signaling-mediated the proliferation and activation of fibroblasts