ArticleCell metabolism2020
Cholesterol Stabilizes TAZ in Hepatocytes to Promote Experimental Non-alcoholic Steatohepatitis.
Article in Cell metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 1 of them a synthesis that pooled it.
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Who cites it
121 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.
- Identification of CXCR4 Upregulation in Diffuse Large B-Cell Lymphoma Associated with Prognostic Significance and Clinicopathological Characteristics.Disease markers · 2022Pooled it
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Precision pathophysiology in steatotic liver disease.Clinical and molecular hepatology · 2026Review
- TRMT10A maintains lipid homeostasis independently of its tRNA mScience China. Life sciences · 2026Article
- Targeting cytokine-like protein FAM3D alleviates atherosclerosis.Cell reports. Medicine · 2026Article
- Targeting hepatic cholesterol sensing to tackle metabolic dysfunction-associated steatohepatitis.The Journal of clinical investigation · 2026Article
- Mechanisms and therapeutic insights into MASH-associated fibrosis.Trends in endocrinology and metabolism: TEM · 2026Review
- Hepatocyte-specific yes-associated protein knockout exacerbates non-alcoholic steatohepatitis by upregulating PCSK9.Journal of gastroenterology · 2026Article
- Liver Stiffness Directs Intrahepatic Cholesterol Accumulation Through YAP/TAZ in Metabolic Dysfunction-Associated Steatotic Liver Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Balancing cholesterol metabolism in the liver and gut: perspectives in health and disease.Nature reviews. Gastroenterology & hepatology · 2026Review
- ZFP36 Alleviates MASLD Through Facilitating TEAD4 mRNA Degradation After Sleeve Gastrectomy.International journal of molecular sciences · 2026Article
- Seipin expression in hepatocytes impairs the assembly of VLDLs and exacerbates steatohepatitis.Journal of lipid research · 2026Article
- Sex-based multiomics analysis uncovers metabolic and molecular mediators linking MASH and atherosclerosis.JHEP reports : innovation in hepatology · 2026Article
- Invited: Longitudinal Assessment of Diets with Varying Carbohydrate-to-Fat Ratios and Fiber Supplementation on Immunometabolic Markers, Liver Function, and Gut Microbiome.The Journal of nutrition · 2026Article
- Cholesterol Overload Drives Hepatic Steatosis by Inhibiting OGT-dependent PPARα O-GlcNAcylation and Transactivation.International journal of biological sciences · 2026Article
- Signaling pathway networks in frozen shoulder fibrosis: from inflammatory initiation to fibrotic progression.Frontiers in medicine · 2026Review
- Urea functions as a risk signal driving astrocyte-mediated neuroinflammation following stroke.Journal of neuroinflammation · 2025Article
- Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025Review
- Mediation analysis of the molecular phenotypes in a severe MASH-like liver injury mouse model.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Cholesterol metabolism on stem cell fate determination: a frontier horizon.Stem cell research & therapy · 2025Review
61 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 8 institutions in 3 countries.
Funding
Abstract
Incomplete understanding of how hepatosteatosis transitions to fibrotic non-alcoholic steatohepatitis (NASH) has limited therapeutic options. Two molecules that are elevated in hepatocytes in human NASH liver are cholesterol, whose mechanistic link to NASH remains incompletely understood, and TAZ, a transcriptional regulator that promotes fibrosis but whose mechanism of increase in NASH is unknown. We now show that increased hepatocyte cholesterol upregulates TAZ and promotes fibrotic NASH. ASTER-B/C-mediated internalization of plasma membrane cholesterol activates soluble adenylyl cyclase (sAC; ADCY10), triggering a calcium-RhoA-mediated pathway that suppresses β-TrCP/proteasome-mediated TAZ degradation. In mice fed with a cholesterol-rich NASH-inducing diet, hepatocyte-specific silencing of ASTER-B/C, sAC, or RhoA decreased TAZ and ameliorated fibrotic NASH. The cholesterol-TAZ pathway is present in primary human hepatocytes, and associations among liver cholesterol, TAZ, and RhoA in human NASH liver are consistent with the pathway. Thus, hepatocyte cholesterol contributes to fibrotic NASH by increasing TAZ, suggesting new targets for therapeutic intervention.
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