ArticleActa pharmacologica Sinica2023
Salvianolic acid B suppresses hepatic fibrosis by inhibiting ceramide glucosyltransferase in hepatic stellate cells.
Article in Acta pharmacologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 33 citations in OpenAlex.
- Immunometabolic pathways in liver fibrosis: current evidence for selected plant-derived metabolites associated with traditional Chinese medicine.Frontiers in pharmacology · 2026Review
- Rubimaillin ameliorates liver fibrosis by triggering the ferroptosis of activated hepatic stellate cells through targeting CPT1A.International journal of biological sciences · 2026Article
- Measles virus reprograms CD4Frontiers in cell and developmental biology · 2026Article
- Cell-specific roles of autophagy in liver fibrosis: implications for targeted pharmacotherapy.Annals of medicine · 2025Review
- Salvianolic Acid B Attenuates Ferroptosis in Acute Kidney Injury by Targeting PRDX5.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Miglustat ameliorates isoproterenol-induced cardiac fibrosis via targeting UGCG.Molecular medicine (Cambridge, Mass.) · 2025Article
- Non-parenchymal cells: key targets for modulating chronic liver diseases.Frontiers in immunology · 2025Review
- Phe-Phe-Based Macroscopic Supramolecular Hydrogel Construction Strategies and Biomedical Applications.Chem & bio engineering · 2024Review
- Advancements in Plant-Based Therapeutics for Hepatic Fibrosis: Molecular Mechanisms and Nanoparticulate Drug Delivery Systems.International journal of molecular sciences · 2024Review
- Review
- UGCG modulates heart hypertrophy through B4GalT5-mediated mitochondrial oxidative stress and the ERK signaling pathway.Cellular & molecular biology letters · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
UDP-glucose ceramide glucosyltransferase (UGCG) is the first key enzyme in glycosphingolipid (GSL) metabolism that produces glucosylceramide (GlcCer). Increased UGCG synthesis is associated with cell proliferation, invasion and multidrug resistance in human cancers. In this study we investigated the role of UGCG in the pathogenesis of hepatic fibrosis. We first found that UGCG was over-expressed in fibrotic livers and activated hepatic stellate cells (HSCs). In human HSC-LX2 cells, inhibition of UGCG with PDMP or knockdown of UGCG suppressed the expression of the biomarkers of HSC activation (α-SMA and collagen I). Furthermore, pretreatment with PDMP (40 μM) impaired lysosomal homeostasis and blocked the process of autophagy, leading to activation of retinoic acid signaling pathway and accumulation of lipid droplets. After exploring the structure and key catalytic residues of UGCG in the activation of HSCs, we conducted virtual screening, molecular interaction and molecular docking experiments, and demonstrated salvianolic acid B (SAB) from the traditional Chinese medicine Salvia miltiorrhiza as an UGCG inhibitor with an IC
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