ArticleNature communications2019
Hepatocyte-specific loss of GPS2 in mice reduces non-alcoholic steatohepatitis via activation of PPARα.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 58 citations in OpenAlex.
- GPS2 regulates embryonic angiogenesis by enhancing endothelial cell survival through stabilizing HOIP.Cell death and differentiation · 2026Article
- Spatial transcriptome mapping identifiesScience advances · 2026Article
- Sex-specific KDM6A-HNF4A-CREBH network controls lipoprotein cholesterol metabolism and atherosclerosis via epigenetic reprograming of hepatocytes.Nature communications · 2026Article
- Nuclear receptor coregulator interactions: beyond the switch.Genes & development · 2026Review
- Concerted Actions of FoxO1 and PPARα in Hepatic Gene Expression and Metabolic Adaptation.Diabetes · 2025Article
- Liquid-liquid phase separation of GPS2-LATS1 promotes colorectal cancer progression by reprogramming lipid metabolism.Oncogene · 2025Article
- SMRT anchors the HDAC3 corepressor complex to chromatin to regulate inflammatory and metabolic pathways in macrophages.Nucleic acids research · 2025Article
- Targeting the chromatin remodeler BAZ2B mitigates hepatic senescence and MASH fibrosis.Nature aging · 2025Article
- Nonproteolytic ubiquitination regulates chromatin occupancy by the NCoR/SMRT/HDAC3 corepressor complex in MCF-7 breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- PPARɑ variant V227A reduces plasma triglycerides through enhanced lipoprotein lipolysis.Journal of lipid research · 2025Article
- PPARα regulates ER-lipid droplet protein Calsyntenin-3β to promote ketogenesis in hepatocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Overexpression of Apolipoprotein A-I Alleviates Insulin Resistance in MASLD Mice Through the PPARα Pathway.International journal of molecular sciences · 2025Article
- Article
- From NAFLD to NASH: Understanding the spectrum of non-alcoholic liver diseases and their consequences.Heliyon · 2024Review
- Nuclear receptor corepressors non-canonically drive glucocorticoid receptor-dependent activation of hepatic gluconeogenesis.Nature metabolism · 2024Article
- A spatiotemporal atlas of mouse liver homeostasis and regeneration.Nature genetics · 2024Article
- Loss ofZoological research · 2024Article
- Nuclear Receptor PPARα as a Therapeutic Target in Diseases Associated with Lipid Metabolism Disorders.Nutrients · 2023Review
- Immunobiology of cancer stem cells and their immunoevasion mechanisms.Molecular biology reports · 2023Review
- FXR Friend-ChIPs in the Enterohepatic System.Seminars in liver disease · 2023Review
Corrections and comments
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Authors and funding
23 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity triggers the development of non-alcoholic fatty liver disease (NAFLD), which involves alterations of regulatory transcription networks and epigenomes in hepatocytes. Here we demonstrate that G protein pathway suppressor 2 (GPS2), a subunit of the nuclear receptor corepressor (NCOR) and histone deacetylase 3 (HDAC3) complex, has a central role in these alterations and accelerates the progression of NAFLD towards non-alcoholic steatohepatitis (NASH). Hepatocyte-specific Gps2 knockout in mice alleviates the development of diet-induced steatosis and fibrosis and causes activation of lipid catabolic genes. Integrative cistrome, epigenome and transcriptome analysis identifies the lipid-sensing peroxisome proliferator-activated receptor α (PPARα, NR1C1) as a direct GPS2 target. Liver gene expression data from human patients reveal that Gps2 expression positively correlates with a NASH/fibrosis gene signature. Collectively, our data suggest that the GPS2-PPARα partnership in hepatocytes coordinates the progression of NAFLD in mice and in humans and thus might be of therapeutic interest.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.