<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(10)</volume><submitter>Andres-Rozas M</submitter><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>Steatotic liver disease can lead to the development of metabolic dysfunction-associated steatohepatitis (MASH), the prevalence of which is rapidly increasing, intensifying the need to find an effective treatment. GTX-11 is a first-in-class drug with anti-inflammatory and antifibrotic properties mediated by the modulation of the transforming growth factor beta pathway. The present study evaluated the effects of GTX-11 on hepatic hemodynamics and liver fibrosis, as well as its underlying mechanisms, in a preclinical model of MASH, and in human precision-cut liver slices (hPCLS).&lt;h4>Methods&lt;/h4>Male Wistar MASH rats received GTX-11 (1 and 10 mg/kg/day) or vehicle, for 14 days (n = 15/group). &lt;i>In vivo&lt;/i> systemic and hepatic hemodynamics, fibrosis, biochemical para</pubmed_abstract><journal>JHEP reports : innovation in hepatology</journal><pagination>101497</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12447985</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>GTX-11 improves portal hypertension, liver fibrosis, and sinusoidal cells phenotype in experimental MASH.</pubmed_title><pmcid>PMC12447985</pmcid><pubmed_authors>Guixe-Muntet S</pubmed_authors><pubmed_authors>Boyer-Diaz Z</pubmed_authors><pubmed_authors>Garcia-Delgado N</pubmed_authors><pubmed_authors>Lozano JJ</pubmed_authors><pubmed_authors>Aristu-Zabalza P</pubmed_authors><pubmed_authors>Fuster C</pubmed_authors><pubmed_authors>Gracia-Sancho J</pubmed_authors><pubmed_authors>Andres-Rozas M</pubmed_authors><pubmed_authors>Ruiz-Canovas E</pubmed_authors><pubmed_authors>Mercade J</pubmed_authors><pubmed_authors>Fernandez-Asensio C</pubmed_authors><pubmed_authors>Bosch J</pubmed_authors></additional><is_claimable>false</is_claimable><name>GTX-11 improves portal hypertension, liver fibrosis, and sinusoidal cells phenotype in experimental MASH.</name><description>&lt;h4>Background &amp; aims&lt;/h4>Steatotic liver disease can lead to the development of metabolic dysfunction-associated steatohepatitis (MASH), the prevalence of which is rapidly increasing, intensifying the need to find an effective treatment. GTX-11 is a first-in-class drug with anti-inflammatory and antifibrotic properties mediated by the modulation of the transforming growth factor beta pathway. The present study evaluated the effects of GTX-11 on hepatic hemodynamics and liver fibrosis, as well as its underlying mechanisms, in a preclinical model of MASH, and in human precision-cut liver slices (hPCLS).&lt;h4>Methods&lt;/h4>Male Wistar MASH rats received GTX-11 (1 and 10 mg/kg/day) or vehicle, for 14 days (n = 15/group). &lt;i>In vivo&lt;/i> systemic and hepatic hemodynamics, fibrosis, biochemical para</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Oct</publication><modification>2026-06-03T17:02:00.402Z</modification><creation>2026-05-30T03:06:23.243Z</creation></dates><accession>S-EPMC12447985</accession><cross_references><pubmed>40980160</pubmed><doi>10.1016/j.jhepr.2025.101497</doi></cross_references></HashMap>