ArticleBiomedical reports2016
Epithelial-mesenchymal transition in liver fibrosis.
Article in Biomedical reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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
71 citing papers in PubMed, 122 citations in OpenAlex.
- A refined MASH-HCC model identifies macrophage Gadd45b as a key orchestrator of inflammation-driven neoplastic progression.Experimental & molecular medicine · 2026Article
- Cannabinoid 2 Receptor Activation Mitigates High-Fat Diet/Streptozotocin-Induced Nonalcoholic Fatty Liver Disease in Diabetic Mice by Modulation of Oxidative Stress, Inflammation, and Fibrosis.ACS pharmacology & translational science · 2026Article
- SULT2B1 promotes cholangiocyte epithelial-mesenchymal transition in biliary atresia: one baby step or a giant leap in the pathogenesis of biliary atresia?Pediatric research · 2026Article
- Single-cell insights into hepatic fibroblasts and stellate cells: heterogeneity in matrix remodelling in development, health, and disease.Npj gut and liver · 2026Review
- Modulation of phosphatase of regenerating liver-1 within placental mesenchymal stem cells instigates the transition between epithelial-to-mesenchymal transition and mesenchymal-to-epithelial transition subsequent to hepatic fibrosis.Clinical and molecular hepatology · 2025Article
- Nucleic acid spheres for treating capillarisation of liver sinusoidal endothelial cells in liver fibrosis.Nature communications · 2025Article
- HIF-1α/LTBP2 axis activate HSCs to promote liver fibrosis by interacting with LOXL1 via the ERK pathway.Cellular and molecular life sciences : CMLS · 2025Article
- HSC-derived exosomal miR-122-5p inhibits EMT and fibrosis of intrahepatic biliary epithelial cells to alleviate primary biliary cholangitis.Frontiers in immunology · 2025Article
- Idiopathic Pulmonary Fibrosis: Review of Current Knowledge.Physiological research · 2024Review
- Hepatocyte Growth Factor Modulates Corneal Endothelial Wound Healing In Vitro.International journal of molecular sciences · 2024Article
- A novel experimental model of MetALD in male mice recapitulates key features of severe alcohol-associated hepatitis.Hepatology communications · 2024Article
- DCDC2 inhibits hepatic stellate cell activation and ameliorates CClScientific reports · 2024Article
- Methylmalonic acid in aging and disease.Trends in endocrinology and metabolism: TEM · 2024Review
- The inhibition of YAP Signaling Prevents Chronic Biliary Fibrosis in the Abcb4Aging and disease · 2024Article
- Regulation of Hepatocellular Carcinoma Epithelial-Mesenchymal Transition Mechanism and Targeted Therapeutic Approaches.Advances in experimental medicine and biology · 2024Review
- Review
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- The Elk-3 target Abhd10 ameliorates hepatotoxic injury and fibrosis in alcoholic liver disease.Communications biology · 2023Article
- Colorectal cancer-derived small extracellular vesicles induce TGFβ1-mediated epithelial to mesenchymal transition of hepatocytes.Cancer cell international · 2023Article
- Oxy210, a Semi-Synthetic Oxysterol, Inhibits Profibrotic Signaling in Cellular Models of Lung and Kidney Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2023Article
11 more citing papers are in PubMed but not listed here.
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
Liver fibrosis is the result of a sustained wound healing response to sustained chronic liver injury, which includes viral, alcoholic and autoimmune hepatitis. Hepatic regeneration is the dominant outcome of liver damage. The outcomes of successful repair are the replacement of dead epithelial cells with healthy epithelial cells, and reconstruction of the normal hepatic structure and function. Prevention of the development of epithelial-mesenchymal transition (EMT) may control and even reverse liver fibrosis. EMT is a critical process for an epithelial cell to undergo a conversion to a mesenchymal phenotype, and is believed to be an inflammation-induced response, which may have a central role in liver fibrosis. The origin of fibrogenic cells in liver fibrosis remains controversial. Numerous studies have investigated the origin of all fibrogenic cells within the liver and the mechanism of the signaling pathways that lead to the activation of EMT programs during numerous chronic liver diseases. The present study aimed to summarize the evidence to explain the possible role of EMT in 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.