ArticleJournal of gastroenterology and hepatology2021
O-GlcNAcylation inhibits hepatic stellate cell activation.
Article in Journal of gastroenterology and hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
6 citing papers in PubMed, 11 citations in OpenAlex.
- The OGT-TFF2 axis mediates intrahepatic crosstalk and MASH pathogenesis.Hepatology (Baltimore, Md.) · 2026Article
- O-GlcNAcylation controls pro-fibrotic transcriptional regulatory signaling in myofibroblasts.Cell death & disease · 2024Article
- Review
- Emerging Role of Protein O-GlcNAcylation in Liver Metabolism: Implications for Diabetes and NAFLD.International journal of molecular sciences · 2023Review
- O-GlycNacylation Remission Retards the Progression of Non-Alcoholic Fatty Liver Disease.Cells · 2022Review
- Pleiotropic actions of IP6K1 mediate hepatic metabolic dysfunction to promote nonalcoholic fatty liver disease and steatohepatitis.Molecular metabolism · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimProtein O-GlcNAcylation is a critical post-translational modification regulating gene expression and fundamental cell functions. O-GlcNAc transferase (OGT) emerged as a key regulator of liver pathophysiology and disease. In this study, we aimed to evaluate the role of OGT in hepatic stellate cells (HSCs) and its consequent role in liver fibrosis.
methodsPrimary HSCs were isolated from C57/B6 mice. Cell morphology and α-SMA immunofluorescence staining were observed under scanning confocal microscope. Transcriptomic profile was evaluated by RNAseq (Illumina). Promoter activity was examined by luciferase and β--Galactosidase reporter assays. Liver fibrosis mouse models were induced either by intraperitoneal injection of CCl
resultsOGT protein expression and protein O-GlcNAcylation were significantly decreased in CCl
conclusionsOur results suggest that OGT functions as a negative regulator of HSC activation by promoting SRF O-GlcNAcylation to protect against liver fibrosis.
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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.