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While molecular\u2010based strategies have been extensively explored for HSC deactivation, clinically effective therapies remain elusive. Previous studies suggest that epithelial\u2010like features of quiescent HSCs are lost upon activation, implying that mesenchymal\u2013epithelial transition (MET) may be a potential therapeutic mechanism for reversing HSC activation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To identify compounds capable of reprogramming HSCs, we screened a library of 1134 FDA\u2010approved drugs using human HSCs (HHSteCs). Morphological changes were quantified by the axial ratio, and functional assays included proliferation, immunofluorescence, Western blotting, and qPCR. Mechanistic analyses focused on microtubule integrity, focal adhesion signalling, and YAP\/TAZ activity. Antifibrotic effects in\u00a0vivo were evaluated using a carbon tetrachloride (CCl\n                      <jats:sub>4<\/jats:sub>\n                      )\u2010induced mouse fibrosis model treated with febantel, the prodrug of fenbendazole.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Five compounds, including taxanes and benzimidazoles, induced epithelial\u2010like morphology and suppressed HSC activation. All shared the ability to disrupt microtubule dynamics. Fenbendazole exerted the strongest effect, reducing mesenchymal markers while restoring E\u2010cadherin expression. Mechanistically, fenbendazole impaired focal adhesion signalling, attenuated YAP\/TAZ activity, and promoted reassembly of adherens junctions, consistent with durable MET\u2010like reprogramming. In\u00a0vivo, febantel administration suppressed \u03b1\u2010SMA and collagen1\u03b11 expression and downregulated fibrogenic genes without altering serum markers of hepatocellular injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings identify microtubule\u2010dynamics inhibitors as potent inducers of MET\u2010like reprogramming in HSCs. Fenbendazole, in particular, promotes HSC inactivation by linking microtubule disruption to focal adhesion and TAZ suppression, while restoring epithelial junction integrity. These insights provide a mechanistic rationale for the antifibrotic potential of microtubule\u2010targeting compounds and highlight benzimidazoles as promising candidates for translational development.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/liv.70780","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T04:01:01Z","timestamp":1783310461000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Microtubule\u2010Targeting Drugs Induce Mesenchymal\u2013Epithelial Transition in Hepatic Stellate Cells"],"prefix":"10.1111","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1040-399X","authenticated-orcid":false,"given":"Hayato","family":"Urushima","sequence":"first","affiliation":[{"name":"Department of Anatomy and Regenerative Biology, Graduate School of Medicine Osaka Metropolitan University  Osaka Japan"},{"name":"Laboratory Animal Facility, Graduate School 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