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. 2020 Oct 16;394(3):533–543. doi: 10.1007/s00210-020-01998-9

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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. 6 — Schematic illustration of mesalazine’s proposed mechanism of antifibrotic action in fibroblasts. Upon stimulation with TGFβ, SMAD2/3, and ERK1/2 are activated, which is reflected by increased protein phosphorylation. Additionally, NFκB translocates from the cytosol to the nucleus, where it may induce fibrotic gene expression. Together, these mechanisms lead to myofibroblast differentiation and collagen deposition, which are hallmarks of fibrosis. Mesalazine treatment inhibits SMAD2/3 and ERK1/2 phosphorylation and prevents nuclear translocation of NFκB, making it an attractive candidate for antifibrotic intervention.