{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang S"],"funding":["NIDDK NIH HHS","NIH R01"],"pagination":["e2405678"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11653607"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(47)"],"pubmed_abstract":["Stressed hepatocytes promote liver fibrosis through communications with hepatic stellate cells (HSCs) during chronic liver injury. However, intra-hepatocyte players that facilitate such cell-to-cell communications are largely undefined. It is previously reported that hepatocyte E4BP4 is potently induced by ER stress and hepatocyte deletion of E4bp4 protects mice from high-fat diet-induced liver steatosis. Here how hepatocyte E4bp4 deficiency impacts the activation of HSCs and the progression toward MASH-associated liver fibrosis is examined. Hepatic E4BP4 is increased in mouse models of NASH diet- or CCl4-induced liver fibrosis. Hepatocyte-specific E4bp4 deletion protected mice against NASH diet-induced liver injury, inflammation, and fibrosis without impacting liver steatosis. Hepatocyte "],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["OPN-Mediated Crosstalk Between Hepatocyte E4BP4 and Hepatic Stellate Cells Promotes MASH-Associated Liver Fibrosis."],"pmcid":["PMC11653607"],"funding_grant_id":["R01 DK121170","P30 DK089503","P30 DK020572","R00 DK077449","R01 DK099593","DK121170.DK099593"],"pubmed_authors":["Zhang G","Wang S","Yang M","Gao J","Tong X","Yin L"],"additional_accession":[]},"is_claimable":false,"name":"OPN-Mediated Crosstalk Between Hepatocyte E4BP4 and Hepatic Stellate Cells Promotes MASH-Associated Liver Fibrosis.","description":"Stressed hepatocytes promote liver fibrosis through communications with hepatic stellate cells (HSCs) during chronic liver injury. However, intra-hepatocyte players that facilitate such cell-to-cell communications are largely undefined. It is previously reported that hepatocyte E4BP4 is potently induced by ER stress and hepatocyte deletion of E4bp4 protects mice from high-fat diet-induced liver steatosis. Here how hepatocyte E4bp4 deficiency impacts the activation of HSCs and the progression toward MASH-associated liver fibrosis is examined. Hepatic E4BP4 is increased in mouse models of NASH diet- or CCl4-induced liver fibrosis. Hepatocyte-specific E4bp4 deletion protected mice against NASH diet-induced liver injury, inflammation, and fibrosis without impacting liver steatosis. Hepatocyte ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2026-06-01T17:38:18.105Z","creation":"2025-04-04T21:43:59.368Z"},"accession":"S-EPMC11653607","cross_references":{"pubmed":["39473081"],"doi":["10.1002/advs.202405678"]}}