{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang H"],"funding":["NIH HHS"],"pagination":["1468"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12898518"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27(3)"],"pubmed_abstract":["Forkhead box protein A3 (FOXA3), also known as hepatocyte nuclear factor 3g (HNF3g), is a member of the FOX family of transcription factors and regulates lipid and glucose metabolism and liver regeneration. Hepatic FOXA3 is reduced in obesity and patients with metabolic dysfunction-associated steatohepatitis (MASH). So far, it remains unknown whether hepatic FOXA3 is essential for regulating lipid metabolism or metabolic dysfunction-associated liver disease (MASLD). In this study, we first investigated whether genetic inactivation of hepatocyte <i>Foxa3</i> affected the development of MASLD/MASH in C57BL/6 mice and then explored whether loss of hepatocyte <i>Foxa3</i> regulated atherosclerosis development in <i>Ldlr</i>-deficient mice. Inactivation of <i>Foxa3</i> in hepatocytes did not af"],"journal":["International journal of molecular sciences"],"pubmed_title":["Loss of Hepatocyte FOXA3 Improves MASH and Atherosclerosis in Hyperlipidemic Ldlr-Deficient Mice."],"pmcid":["PMC12898518"],"funding_grant_id":["1R01DK121548-04","1R01DK118805-04"],"pubmed_authors":["Gopoju R","Hu S","Gunawardana L","Zhang Y","Wang H","Wang X","Wang J","Lin L","Yin L"],"additional_accession":[]},"is_claimable":false,"name":"Loss of Hepatocyte FOXA3 Improves MASH and Atherosclerosis in Hyperlipidemic Ldlr-Deficient Mice.","description":"Forkhead box protein A3 (FOXA3), also known as hepatocyte nuclear factor 3g (HNF3g), is a member of the FOX family of transcription factors and regulates lipid and glucose metabolism and liver regeneration. Hepatic FOXA3 is reduced in obesity and patients with metabolic dysfunction-associated steatohepatitis (MASH). So far, it remains unknown whether hepatic FOXA3 is essential for regulating lipid metabolism or metabolic dysfunction-associated liver disease (MASLD). In this study, we first investigated whether genetic inactivation of hepatocyte <i>Foxa3</i> affected the development of MASLD/MASH in C57BL/6 mice and then explored whether loss of hepatocyte <i>Foxa3</i> regulated atherosclerosis development in <i>Ldlr</i>-deficient mice. Inactivation of <i>Foxa3</i> in hepatocytes did not af","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-07-09T10:21:29.211Z","creation":"2026-07-09T10:18:54.959Z"},"accession":"S-EPMC12898518","cross_references":{"pubmed":["41683889"],"doi":["10.3390/ijms27031468"]}}