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Although adipose-derived stem cells (ADSCs) transplantation can alleviate hepatic fibrosis, their mechanism remains unclear. Accordingly, we explored the efficacy and mechanisms behind ADSCs transplantation in two LF models.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"sec002\">\n<jats:title>Methodology<\/jats:title>\n<jats:p>The carbon tetrachloride (CCl<jats:sub>4<\/jats:sub>)-induced liver injury and <jats:italic>Echinococcus multilocularis<\/jats:italic> (<jats:italic>E. multilocularis<\/jats:italic>) infection models were established, and ADSCs were transplanted. Mouse liver samples were harvested and analyzed histologically. Expression levels of fibrosis and senescence-related proteins were analyzed by immunohistochemistry. Hepatic stellate cells (HSCs) activation and cell senescence protein expression were evaluated via western blotting. Co-localization expression was determined by immunofluorescence. To assess the cellular senescence degree, we utilized senescence-associated \u03b2-galactosidase (SA-\u03b2-Gal) staining.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"sec003\">\n<jats:title>Result<\/jats:title>\n<jats:p>In the CCl<jats:sub>4<\/jats:sub>-induced LF mouse model, the liver surface exhibited a rough texture. The hematoxylin and eosin (H&amp;E) staining revealed hepatic parenchymal cell destruction accompanied by pseudolobule formation and fibrosis in the portal area. In the <jats:italic>E. multilocularis<\/jats:italic> infection model, multiple white foci were on the liver surface. The H&amp;E staining revealed massive inflammatory cell infiltration around the foci with severe fibrosis, and Sirius Red confirmed collagen deposition; both had elevated HSCs activation (\u03b1-SMA expression). After ADSCs transplantation, the collagen deposition and HSCs activation significantly diminished, while the cellular senescence levels increased. Immunofluorescence co-localization of p21 and a-SMA showed that transplantation of ADSCs promoted senescence of activated HSCs (aHSCs). <jats:italic>In vitro<\/jats:italic> co-culture had similar results, accompanied by expression changes and TGF-\u03b2\/Smad signaling inhibition.<\/jats:p>\n<\/jats:sec>\n<jats:sec id=\"sec004\">\n<jats:title>Conclusion<\/jats:title>\n<jats:p>Our findings indicate that ADSCs transplantation can mitigate fibrosis by inducing the senescence of aHSCs and reducing collagen production.<\/jats:p>\n<\/jats:sec>","DOI":"10.1371\/journal.pntd.0013094","type":"journal-article","created":{"date-parts":[[2025,5,22]],"date-time":"2025-05-22T17:34:57Z","timestamp":1747935297000},"page":"e0013094","update-policy":"https:\/\/doi.org\/10.1371\/journal.pntd.corrections_policy","source":"Crossref","is-referenced-by-count":6,"title":["ADSCs attenuate Liver fibrosis via inducing HSC senescence: validation in dual-etiology 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