{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(8)"],"submitter":["Meng Z"],"pubmed_abstract":["<h4>Background & aims</h4>Cellular heterogeneity of innate immune cells, such as macrophages, in the liver is a hallmark of metabolic dysfunction-associated steatohepatitis (MASH) pathogenesis. However, the mechanisms shaping liver macrophage heterogeneity and function during disease progression remain poorly understood.<h4>Methods</h4>Control or myeloid-specific <i>Tgfbr1</i> knockout mice (n = 9-12 per group) were fed a 12-week choline-deficient, amino acid-defined high-fat diet (CDA-HFD) or a 20-week GAN diet (40% fat, 22% fructose, 2% cholesterol). Liver tissue was analyzed using histopathology, quantitative PCR, immunoblotting, flow cytometry, and RNA sequencing (RNA-seq). Bulk RNA-seq (n = 3 per group) and single-nucleus RNA-seq were performed to investigate transcriptional reprogram"],"journal":["JHEP reports : innovation in hepatology"],"pagination":["101488"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12284356"],"repository":["biostudies-literature"],"pubmed_title":["Myeloid TGF-β signaling shapes liver macrophage heterogeneity and metabolic liver disease pathogenesis."],"pmcid":["PMC12284356"],"pubmed_authors":["Lee YT","Zhou L","Qiu X","Lin JD","Li S","Chen Z","Lu Y","Gallagher KA","Levi B","Meng Z","Liu T"],"additional_accession":[]},"is_claimable":false,"name":"Myeloid TGF-β signaling shapes liver macrophage heterogeneity and metabolic liver disease pathogenesis.","description":"<h4>Background & aims</h4>Cellular heterogeneity of innate immune cells, such as macrophages, in the liver is a hallmark of metabolic dysfunction-associated steatohepatitis (MASH) pathogenesis. However, the mechanisms shaping liver macrophage heterogeneity and function during disease progression remain poorly understood.<h4>Methods</h4>Control or myeloid-specific <i>Tgfbr1</i> knockout mice (n = 9-12 per group) were fed a 12-week choline-deficient, amino acid-defined high-fat diet (CDA-HFD) or a 20-week GAN diet (40% fat, 22% fructose, 2% cholesterol). Liver tissue was analyzed using histopathology, quantitative PCR, immunoblotting, flow cytometry, and RNA sequencing (RNA-seq). Bulk RNA-seq (n = 3 per group) and single-nucleus RNA-seq were performed to investigate transcriptional reprogram","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-03-16T04:08:17.116Z","creation":"2025-08-14T03:05:50.92Z"},"accession":"S-EPMC12284356","cross_references":{"pubmed":["40704067"],"doi":["10.1016/j.jhepr.2025.101488"]}}