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. 2019 Nov 12;17:145. doi: 10.1186/s12964-019-0455-y

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — Injury-induced epithelial and interstitial Notch1 activity contributes to myofibroblastic phenotype and fibrosis. Injury stimulates the activation of the Notch1 signalling pathway in TECs and fibroblasts. Activated Notch1 signalling starts with a TGF-β1/Smad2/3 signalling cascade, which induces the EMT and FMD response, promotes myofibroblastic phenotype and ECM deposition, and results in interstitial fibrosis. Pharmacologic or genetic blockade of Notch1 signalling decreases TGF-β1 expression and abolishes injury-mediated EMT/FMD, myofibroblastic phenotype and fibrosis