{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["16"],"submitter":["Murphy WA"],"pubmed_abstract":["<h4>Introduction</h4>Metabolic dysfunction-associated steatotic liver disease (MASLD) is estimated to affect ∼30% of adults globally. The progressive form of MASLD, metabolic dysfunction-associated steatohepatitis (MASH), is a leading cause of chronic liver disease. MASH is marked by hepatocellular fat accumulation (steatosis), ballooning, and inflammation. Although many <i>in vitro</i> and <i>in vivo</i> models replicate MASH pathophysiology, no <i>in vitro</i> hepatocyte MASH model has been evaluated for its ability to reflect clinically observed changes in drug metabolizing enzymes (DMEs) and transporters. In this study, we addressed this gap by developing a model using sandwich-cultured human hepatocytes (SCHH) that mimics both MASH pathophysiology and alterations in DME and transporte"],"journal":["Frontiers in pharmacology"],"pagination":["1664808"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12832903"],"repository":["biostudies-literature"],"pubmed_title":["Development of an <i>in vitro</i> metabolic dysfunction-associated steatohepatitis model to investigate altered drug metabolizing enzymes, transport proteins, and hepatobiliary disposition."],"pmcid":["PMC12832903"],"pubmed_authors":["Loop MS","Fallon JK","Murphy WA","Kyburz S","Kralj T","Brouwer KLR","Ho H","Tiley JB"],"additional_accession":[]},"is_claimable":false,"name":"Development of an <i>in vitro</i> metabolic dysfunction-associated steatohepatitis model to investigate altered drug metabolizing enzymes, transport proteins, and hepatobiliary disposition.","description":"<h4>Introduction</h4>Metabolic dysfunction-associated steatotic liver disease (MASLD) is estimated to affect ∼30% of adults globally. The progressive form of MASLD, metabolic dysfunction-associated steatohepatitis (MASH), is a leading cause of chronic liver disease. MASH is marked by hepatocellular fat accumulation (steatosis), ballooning, and inflammation. Although many <i>in vitro</i> and <i>in vivo</i> models replicate MASH pathophysiology, no <i>in vitro</i> hepatocyte MASH model has been evaluated for its ability to reflect clinically observed changes in drug metabolizing enzymes (DMEs) and transporters. In this study, we addressed this gap by developing a model using sandwich-cultured human hepatocytes (SCHH) that mimics both MASH pathophysiology and alterations in DME and transporte","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-06-15T06:24:02.784Z","creation":"2026-06-15T03:08:36.797Z"},"accession":"S-EPMC12832903","cross_references":{"pubmed":["41601959"],"doi":["10.3389/fphar.2025.1664808"]}}