ArticleCytotechnology2019
TGF-β1 signaling activates hepatic stellate cells through Notch pathway.
Article in Cytotechnology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- miR-372-3p represses hepatic stellate cell activation via the RhoC/ROCK pathway.Cytotechnology · 2025Article
- Lipopolysaccharide-binding protein (LBP): a prognostic biomarker for gastric cancer linked to immune infiltration.BMC gastroenterology · 2025Article
- The Complex Interplay of TGF-β and Notch Signaling in the Pathogenesis of Fibrosis.International journal of molecular sciences · 2024Review
- Immunosuppressive tumor microenvironment in the progression, metastasis, and therapy of hepatocellular carcinoma: from bench to bedside.Experimental hematology & oncology · 2024Review
- A detailed overview of quercetin: implications for cell death and liver fibrosis mechanisms.Frontiers in pharmacology · 2024Review
- ATG16L1 Depletion-Mediated Activation of the TRAF1 Signaling in Macrophages Aggravates Liver Fibrosis.Mediators of inflammation · 2024Article
- Pericytes: jack-of-all-trades in cancer-related inflammation.Frontiers in pharmacology · 2024Review
- BM-MSCs overexpressing the Numb enhance the therapeutic effect on cholestatic liver fibrosis by inhibiting the ductular reaction.Stem cell research & therapy · 2023Article
- A Microfluidic Device for Long-Term Maintenance of Organotypic Liver Cultures.Advanced materials technologies · 2023Article
- F-box and WD repeat domain containing 7 inhibits the activation of hepatic stellate cells by degrading delta-like ligand 1 to block Notch signaling pathway.Open medicine (Warsaw, Poland) · 2023Article
- Characterization of human stem cell-derived hepatic stellate cells and liver sinusoidal endothelial cells during extendedFrontiers in bioengineering and biotechnology · 2023Article
- Jagged-1/Notch Pathway and Key Transient Markers Involved in Biliary Fibrosis duringTropical medicine and infectious disease · 2022Article
- RO4929097, a Selective γ-Secretase Inhibitor, Inhibits Subretinal Fibrosis Via Suppressing Notch and ERK1/2 Signaling in Laser-Induced Mouse Model.Investigative ophthalmology & visual science · 2022Article
- DNA methylation profile of liver of mice conceived byJournal of developmental origins of health and disease · 2022Article
- Development of human iPSC-derived quiescent hepatic stellate cell-like cells for drug discovery and in vitro disease modeling.Stem cell reports · 2021Article
- Extra- and Intra-Cellular Mechanisms of Hepatic Stellate Cell Activation.Biomedicines · 2021Review
- Mast Cells Induce Ductular Reaction Mimicking Liver Injury in Mice Through Mast Cell-Derived Transforming Growth Factor Beta 1 Signaling.Hepatology (Baltimore, Md.) · 2021Article
- Astrocyte-Derived TGFβ1 Facilitates Blood-Brain Barrier Function via Non-Canonical Hedgehog Signaling in Brain Microvascular Endothelial Cells.Brain sciences · 2021Article
- Activation of Pancreatic Stellate Cells Is Beneficial for Exocrine but Not Endocrine Cell Differentiation in the Developing Human Pancreas.Frontiers in cell and developmental biology · 2021Article
- The Role of RECK in Hepatobiliary Neoplasia Reveals Its Therapeutic Potential in NASH.Frontiers in endocrinology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatic stellate cells (HSCs), as the most important stromal cells in the liver microenvironment, play crucial roles in hepatic fibrosis, hepatocellular carcinoma, liver regeneration and fetal liver development after transdifferentiating into myofibroblasts (MFs). Transforming growth factor β1 (TGF-β1), as an important polyergic cytokine, is involved in HSCs activation process. However, the specific mechanisms of HSCs transdifferentiation process are not clearly demonstrated. Here we added exogenous recombinant TGF-β1 protein and transforming growth factor β receptor 1 (TGF-βR1) inhibitor SB431542 into mouse HSCs to detect the detailed impact of TGF-β1 signaling on HSCs activation. TGF-β1 signaling significantly increased phosphorylated (P)-Smad2/3 level and promoted Smad2/3 translocation from the cytoplasm to the nucleus, which also caused transdifferentiation of HSCs into MFs. Importantly, TGF-β1 signaling also resulted in high expression of Notch pathway markers Notch1, Jagged1, Hes1 in HSCs. In contrast, expression of those above markers in mouse HSCs were obviously decreased after hampering TGF-β1 signaling via TGF-βR1 inhibitor SB431542. To further examine the effect of Notch pathway on HSCs activation process, TGF-β1-stimulated HSCs and control HSCs were treated with or without LY450139, a specific inhibitor of Notch pathway. LY450139 evidently decreased the expression of Notch1 and MFs marker α-smooth muscle actin (α-SMA) expression in HSCs. These above results may provide a novel insight that TGF-β1 signaling controls HSCs activation process through regulating the expression of Notch pathway markers.
Indexed as
Identifiers
What OpenQuestion holds
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.