ArticleHepatology research : the official journal of the Japan Society of Hepatology2011
Epigenetic cell fate regulation of hepatic stellate cells.
Article in Hepatology research : the official journal of the Japan Society of Hepatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The trial behind it
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Regulation of Hepatic Stellate Cell Phenotypes in Metabolic Dysfunction-Associated Steatohepatitis.Gastroenterology · 2025Review
- Butyrate inhibits histone deacetylase 2 expression to alleviate liver fibrosis in biliary atresia.BMC pediatrics · 2025Article
- Natural medicines for treating liver fibrosis by modulating post-translational modifications.Frontiers in pharmacology · 2025Review
- Alcohol-Associated Liver Disease Outcomes: Critical Mechanisms of Liver Injury Progression.Biomolecules · 2024Review
- Effective delivery of osteopontin small interference RNA using exosomes suppresses liver fibrosisFrontiers in pharmacology · 2022Article
- Analysis of key genes and related transcription factors in liver fibrosis based on bioinformatic technology.International journal of clinical and experimental pathology · 2021Article
- Hepatocyte Injury and Hepatic Stem Cell Niche in the Progression of Non-Alcoholic Steatohepatitis.Cells · 2020Review
- Article
- Thrombin cleavage of osteopontin controls activation of hepatic stellate cells and is essential for liver fibrogenesis.Journal of cellular physiology · 2019Article
- miR-193a/b-3p relieves hepatic fibrosis and restrains proliferation and activation of hepatic stellate cells.Journal of cellular and molecular medicine · 2019Article
- Antifibrotics in liver disease: are we getting closer to clinical use?Hepatology international · 2019Review
- A cAbl-MRTF-A Feedback Loop Contributes to Hepatic Stellate Cell Activation.Frontiers in cell and developmental biology · 2019Article
- ThymosinOxidative medicine and cellular longevity · 2018Article
- Dkk1: A key molecule in joint remodelling and fibrosis.Mediterranean journal of rheumatology · 2017Review
- Tricyclic Antidepressants Promote Ceramide Accumulation to Regulate Collagen Production in Human Hepatic Stellate Cells.Scientific reports · 2017Article
- [Effect of high fat on fibrosis in rat hepatic stellate cells].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2016Article
- The role of immune cells in metabolism-related liver inflammation and development of non-alcoholic steatohepatitis (NASH).Reviews in endocrine & metabolic disorders · 2016Review
- Epigenetic Changes during Hepatic Stellate Cell Activation.PloS one · 2015Article
- New Approaches for Studying Alcoholic Liver Disease.Current pathobiology reports · 2014Article
- Novel modulators of hepatosteatosis, inflammation and fibrogenesis.Hepatology international · 2014Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Research in the past three decades has identified key mediators and signaling mechanisms responsible for myofibroblastic transdifferentiation (MTD) of hepatic stellate cells (HSC), the pivotal event in liver fibrogenesis. Yet, fundamental understanding of the MTD from the viewpoint of cell fate or lineage regulation has been elusive. Recent studies using genetic cell fate mapping techniques demonstrate HSC are derived from mesoderm and at least in part via septum transversum and mesothelium. HSC express markers for different cell types derived from multipotent mesenchymal progenitors. A regulatory commonality between differentiation of adipocytes and that of HSC is shown, and a shift from adipogenic to myogenic or neuronal phenotype characterizes HSC MTD. Central to this shift is a loss of expression of the master adipogenic regulator peroxisome proliferator activated receptor-γ (PPAR-γ). Restored expression of PPAR-γ and/or other adipogenic transcription factors reverses myofibroblastic HSC to differentiated cells. In MTD, Pparγ is epigenetically repressed by induction of methyl-CpG binding protein 2 and its enrichment to the promoter and polycomb repressive complex-facilitated histone H3 lysine 27 di/tri-methylation at the 3' exons. Blocking canonical wingless-related MMTV integration site (Wnt) signaling in myofibroblastic HSC with the co-receptor antagonist Dickkopf-1, abrogates these epigenetic mechanisms, restores PPAR-γ expression and HSC differentiation. Necdin, a melanoma antigen family protein, is identified as an upstream mediator for induction of the canonical Wnt10b and consequent Pparγ repression and HSC MTD. The identified morphogen-induced epigenetic regulation of Pparγ and HSC fate may serve as a novel target for manipulation of liver fibrosis and mesenchymal-epithelial interactions in liver regeneration.
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Registered trials
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.