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. 2021 Oct 26;7:314. doi: 10.1038/s41420-021-00679-7

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© The Author(s) 2021

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 — β-catenin is a target gene of Hh/Gli2 signalling. Hh signalling can enhance Wnt signalling by inducing the expression of β-catenin in the colon during IBD and CAC. Epithelial Ihh and Shh upregulate the expression of Wnt2B in intestinal mesenchymal cells during chronic intestinal inflammation. The subepithelial Gli1-positive mesenchymal cells express high levels of Wnt2B. Dhh-activated Hh signalling positively regulates epithelial cell-produced Wnt2B expression following IEC injury and regeneration. Gli1-expressing mesenchymal cells serve as a reserve Wnt source during recovery from DSS-induced colitis in mice, thereby enhancing Wnt signalling. Shh is a target gene of NK-κB and can be induced by the activation of NK-κB in inflamed intestinal epithelial cells. NK-κB mediates NOD2-iNOS/NO-NUMB-mediated Shh signalling activation, which plays a role in modulating inflammatory responses in IBD. TNF-a/NF-κB signalling promotes the activation of Hh/Gli1/Gli2 signalling in DSS- or AOM/DSS-induced colitis. Arrows and blunt ends indicate activation and inhibition, respectively. The blue arrows indicate a special condition where Gli1 is overexpressed in mesenchymal cells. NOD2 the nucleotide-binding oligomerization domain 2, iNOS inducible nitric-oxide synthase, NO nitric oxide, NF-κB nuclear factor-kappaB, Ihh Indian hedgehog, Dhh Desert hedgehog, Shh Sonic hedgehog, Ptch Patched, Smo Smoothened, Gli1 Glioma-associated oncogene 1, Gli2 Glioma-associated oncogene 2, AOM-DSS azoxymethane and dextran sodium sulphate, JMJD2D jumonji domain-containing protein 2D.