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. 2024 Jan 16;14:1396. doi: 10.1038/s41598-023-49240-9

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© The Author(s) 2024

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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A schematic presentation of the importance of 5-HT signalling in liver fibrosis. Both FFA and 5-HT induced fibrosis in the spheroids, comprised of PHH and NPC, presumably through the activation of hepatic stellate cells. Fibrotic phenotype presented with increased deposition of COL1A1, as well as with increased production of TGF-β1, vimentin, and α-SMA. 5-HT receptor antagonists were tested for their anti-fibrotic capacity. FFA-induced fibrosis was decreased by all four tested 5-HT receptor antagonists. However, ketanserin showed the strongest anti-fibrotic characteristics. Anti-fibrotic activity of the tested 5-HT_2A antagonists can be blocked by knocking down the receptor. Results of the study emphasize the importance of 5-HT signalling in liver fibrosis development, as well as warrant further search for novel targets for liver fibrosis treatment among members of the 5-HT pathway. 5-HT serotonin, COL1A1 collagen, type I, α1, FFA free fatty acids, NPC non-parenchymal cells, PHH primary human hepatocytes, TGF-β1 transforming growth factor beta 1. Created with BioRender.com.