ArticleScientific reports2019
Transcriptional regulation of Hepatic Stellate Cell activation in NASH.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Mapping the global research output of Traditional Chinese Medicine in the treatment of metabolic dysfunction-associated steatotic liver disease: a comprehensive bibliometric analysis based on multiple databases (2000-2025).Frontiers in medicine · 2026Pooled it
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- A Conserved Macrophage-to-Hepatic Stellate Cell PDGF Axis in Human MASH Identified by Multi-Cohort sc/snRNA-Seq Re-Analysis.International journal of molecular sciences · 2026Article
- NAT10 promotes the activation of hepatic stellate cells by modulating the TGF-β1-ac4C-COL1A1 axis.Hepatology international · 2026Article
- ETS1 suppresses hepatic stellate cell activation and liver fibrosis.JCI insight · 2025Article
- The Dual Role of RUNX1 in Inflammation-Driven Age-Related Diseases: From Molecular Mechanisms to Clinical Translation.Biomedicines · 2025Review
- Hepatic stellate cells in liver fibrosis: From biology to pathology.Open veterinary journal · 2025Review
- Regulation of Hepatic Stellate Cell Phenotypes in Metabolic Dysfunction-Associated Steatohepatitis.Gastroenterology · 2025Review
- Increased matrix stiffness promotes fibrogenesis of hepatic stellate cells through AP-1-induced chromatin priming.Communications biology · 2025Article
- Autocrine GDF10 Inhibits Hepatic Stellate Cell Activation via BMPR2/ALK3 Receptor to Prevent Liver Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Luteolin-7-diglucuronide, a novel PTP1B inhibitor, ameliorates hepatic stellate cell activation and liver fibrosis in mice.Acta pharmacologica Sinica · 2025Article
- The microenvironment in the development of MASLD-MASH-HCC and associated therapeutic in MASH-HCC.Frontiers in immunology · 2025Review
- Runt-related transcription factors: from pathogenesis to therapeutic targets in multiple-organ fibrosis.Frontiers in cell and developmental biology · 2025Review
- Natural medicines for treating liver fibrosis by modulating post-translational modifications.Frontiers in pharmacology · 2025Review
- Suppression of hepatic steatosis in non-alcoholic steatohepatitis model by modified Xiaoyao San formula: Evidence, mechanisms and perspective.World journal of hepatology · 2024Article
- The effects of simvastatin-loaded nanoliposomes on human multilineage liver fibrosis microtissue.Journal of cellular and molecular medicine · 2024Article
- O-GlcNAcylation controls pro-fibrotic transcriptional regulatory signaling in myofibroblasts.Cell death & disease · 2024Article
- Orphan receptor GPR176 in hepatic stellate cells exerts a profibrotic role in chronic liver disease.JHEP reports : innovation in hepatology · 2024Article
- Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis.Immunity · 2024Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic steatohepatitis (NASH) signified by hepatic steatosis, inflammation, hepatocellular injury, and fibrosis is a growing cause of chronic liver disease, cirrhosis, and hepatocellular carcinoma. Hepatic fibrosis resulting from accumulation of extracellular matrix proteins secreted by hepatic myofibroblasts plays an important role in disease progression. Activated hepatic stellate cells (HSCs) have been identified as the primary source of myofibroblasts in animal models of hepatotoxic liver injury; however, so far HSC activation and plasticity have not been thoroughly investigated in the context of NASH-related fibrogenesis. Here we have determined the time-resolved changes in the HSC transcriptome during development of Western diet- and fructose-induced NASH in mice, a NASH model recapitulating human disease. Intriguingly, HSC transcriptional dynamics are highly similar across disease models pointing to HSC activation as a point of convergence in the development of fibrotic liver disease. Bioinformatic interrogation of the promoter sequences of activated genes combined with loss-of-function experiments indicates that the transcriptional regulators ETS1 and RUNX1 act as drivers of NASH-associated HSC plasticity. Taken together, our results implicate HSC activation and transcriptional plasticity as key aspects of NASH pathophysiology.
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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.