ReviewJournal of gastroenterology2014
TGF-β signal shifting between tumor suppression and fibro-carcinogenesis in human chronic liver diseases.
Review in Journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 25 citations in OpenAlex.
- Comparative clinical study between the effect of fenofibrate alone and its combination with pentoxifylline on biochemical parameters and liver stiffness in patients with non-alcoholic fatty liver disease.Hepatology international · 2015Trial
- Unveiling the prognostic power of FIB-4 index: a new frontier in heart failure mortality.European journal of medical research · 2025Article
- Proteomic analysis of DEN and CClScientific reports · 2024Article
- Genetic dominance of transforming growth factor-β1 polymorphisms in chronic liver disease.Frontiers in immunology · 2022Article
- The mRNA-miRNA-lncRNA Regulatory Network and Factors Associated with Prognosis Prediction of Hepatocellular Carcinoma.Genomics, proteomics & bioinformatics · 2021Article
- DNA Methylation of TGFβ Target Genes: Epigenetic Control of TGFβ Functional Duality in Liver Cancer.Cells · 2021Article
- The EBV-Encoded Oncoprotein, LMP1, Recruits and Transforms Fibroblasts via an ERK-MAPK-Dependent Mechanism.Pathogens (Basel, Switzerland) · 2021Article
- TGF-β Signaling in Liver, Pancreas, and Gastrointestinal Diseases and Cancer.Gastroenterology · 2021Review
- Smad3 gene C-terminal phosphorylation site mutation aggravates CClJournal of cellular and molecular medicine · 2020Article
- Review
- Stevioside inhibits experimental fibrosis by down-regulating profibrotic Smad pathways and blocking hepatic stellate cell activation.Basic & clinical pharmacology & toxicology · 2019Article
- miR-888 functions as an oncogene and predicts poor prognosis in colorectal cancer.Oncology letters · 2018Article
- Estrogen related receptor alpha triggers the migration and invasion of endometrial cancer cells via up regulation of TGFB1.Cell adhesion & migration · 2018Article
- Transforming Growth Factor-beta 1 Involved in the Pathogenesis of Endometriosis through Regulating Expression of Vascular Endothelial Growth Factor under Hypoxia.Chinese medical journal · 2017Article
- Mesenchymal Cell Reprogramming in Experimental MPLW515L Mouse Model of Myelofibrosis.PloS one · 2017Article
- Involvement of TGF-β1/Smad3 Signaling in Carbon Tetrachloride-Induced Acute Liver Injury in Mice.PloS one · 2016Article
- MAPK inhibitors modulate Smad2/3/4 complex cyto-nuclear translocation in myofibroblasts via Imp7/8 mediation.Molecular and cellular biochemistry · 2015Article
- EVI1, a target gene for amplification at 3q26, antagonizes transforming growth factor-β-mediated growth inhibition in hepatocellular carcinoma.Cancer science · 2015Article
- Axl activates autocrine transforming growth factor-β signaling in hepatocellular carcinoma.Hepatology (Baltimore, Md.) · 2015Article
- Alcohol induced hepatic degeneration in a hepatitis C virus core protein transgenic mouse model.International journal of molecular sciences · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perturbation of transforming growth factor (TGF)-β signaling in hepatocytes persistently infected with hepatitis viruses promotes both fibrogenesis and carcinogenesis (fibro-carcinogenesis). Insights into hepatocytic fibro-carcinogenesis have emerged from recent detailed analyses of context-dependent and cell type-specific TGF-β signaling processes directed by multiple phosphorylated forms (phospho-isoforms) of Smad mediators. In the course of hepatitis virus-related chronic liver diseases, chronic inflammation, ongoing viral infection, and host genetic/epigenetic alterations additively shift hepatocytic Smad phospho-isoform signaling from tumor suppression to fibro-carcinogenesis, accelerating liver fibrosis and increasing risk of hepatocellular carcinoma (HCC). After successful antiviral therapy, patients with chronic hepatitis can experience less risk of HCC occurrence by reversing Smad phospho-isoform signaling from fibro-carcinogenesis to tumor suppression. However, patients with cirrhosis can still develop HCC owing to sustained, intense fibro-carcinogenic signaling. Recent progress in understanding Smad phospho-isoform signaling should permit use of Smad phosphorylation as a tool predicting the likelihood of liver disease progression, and as a biomarker for assessing the effectiveness of interventions aimed at reducing fibrosis and cancer risk.
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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.