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. 2022 Feb 8;8:51. doi: 10.1038/s41420-022-00846-4

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© The Author(s) 2022

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. 8 — In a healthy liver, ECM1 interacts with αV integrin to maintain the latent state of TGF-β. After liver injury, ECM1 levels are decreased, leading to the activation of TGF-β by α_V integrin, which in turn activates HSCs through the TGF-β/Smad pathway. ECM1-HF-MSCs can inhibit the activation of TGF-β through exogenous supplementation with ECM1, which in turn affects the activation of HSCs, thereby alleviating LC.