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. 2020 Jul 3;43(6):593–629. doi: 10.1007/s12272-020-01247-w

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© The Author(s) 2020

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. 4 — Mechanism of hepatoprotective activity of mistletoe, TGFβ/Smad pathway. TGFβ1 binds to its receptor, which consists of two type I and two type II subunits. Type II subunit phosphorylates type I subunit, which then phosphorylates Smad 2 and Smad 3. Phosphorylated Smad 2 and Smad 3 bind with Smad 4 and together they move into the nucleus to regulate expression of target genes. Smad 7 is an inhibitory Smad that negatively regulates Smad 2/3 activation. In vivo study showed that mistletoe alkaloid fractions downregulate TGF-β1, TGF-β1 receptor, phosphorylated Smad 2 and α-SMA proteins as well as downregulate the mRNA levels of TGF-β1, collagen I and TIMP-1. In contrast, Smad 7 level is upregulated. In vitro study showed that mistletoe alkaloid fractions induce Smad 7 expression and inhibit the expression of α-SMA, TGFβ1, TGF-β1 receptor, Smad 2 and TIMP-1