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. 2025 Jan 29;9(2):e0614. doi: 10.1097/HC9.0000000000000614

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Copyright © 2025 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Association for the Study of Liver Diseases.

This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0/

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Identification of antifibrotic candidates in the secretomes of HepLPCs. (A) Volcano plot analysis of differential protein expression in HepLPC-secretomes (HepLPC-scrtms) compared to PHH-secretomes (PHH-scrtms). Red plots indicate upregulated proteins in HepLPC-scrtms, while blue plots indicate downregulated proteins. (B) Pie chart depicting the subcellular locations of proteins upregulated in HepLPC-scrtms. (C) Analysis of 54 proteins showing >5-fold higher abundance in HepLPC-scrtms compared to PHH-scrtms. Protein abundance was determined by normalizing the number of identified peptides in tandem mass tag analyses. (D) Gene ontology chart illustrating biological processes associated with the 54 identified proteins. (E) Potential network interactions of proteins involved in growth factor activity, cytokine activity, and receptor-ligand activity with the JAK-STAT pathway. (F) Immunoblot analysis of cell-free secretomes showing the secretion levels of CSF1, AREG, FGF19, EDN1, and LIF. Abbreviations: AREG, amphiregulin; ER, endoplasmic reticulum; FGF19, fibroblast growth factor 19; HepLPCs, hepatocyte-derived liver progenitor-like cells; LIF, leukemia inhibitory factor; PHHs, primary hepatocytes.