ArticleHepatology communications2019
Liver Proliferation Is an Essential Driver of Fibrosis in Mouse Models of Nonalcoholic Fatty Liver Disease.
Article in Hepatology communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 30 citations in OpenAlex.
- Effects of tesamorelin on hepatic transcriptomic signatures in HIV-associated NAFLD.JCI insight · 2020Trial
- Longchai Decoction Treated the Fibrosis of Liver Induced by CClJournal of cellular and molecular medicine · 2026Article
- Investigation of a Two-Patch Within-Host Model of Hepatitis B Viral Infection.Bulletin of mathematical biology · 2025Article
- From surgery to recovery: Measuring success through quality of life and functional improvements after cardiac surgery.World journal of cardiology · 2025Article
- Current Treatment Regimens and Promising Molecular Therapies for Chronic Hepatobiliary Diseases.Biomolecules · 2025Review
- Hepatocyte-specific angiotensinogen deficiency inhibits Western diet-induced liver steatosis with suppression of cell division in mice.Global translational medicine · 2025Article
- Mouse Models for the Study of Liver Fibrosis RegressionJournal of clinical and translational hepatology · 2024Review
- Article
- Loss of CEACAM1 in hepatocytes causes hepatic fibrosis.European journal of clinical investigation · 2024Article
- Exploring the association between dietary fiber intake and hepatic steatosis: insights from NHANES.BMC gastroenterology · 2024Article
- Multi-omics analysis of a fatty liver model using human hepatocyte chimeric mice.Scientific reports · 2024Article
- Genetic Ablation of C/EBPα-p300 Pathway Blocks Development of Obese Pregnancy Associated Liver Disorders in Offspring.Cellular and molecular gastroenterology and hepatology · 2024Article
- Preclinical Models and Promising Pharmacotherapeutic Strategies in Liver Fibrosis: An Update.Current issues in molecular biology · 2023Review
- Modulating sphingosine 1-phosphate receptor signaling skews intrahepatic leukocytes and attenuates murine nonalcoholic steatohepatitis.Frontiers in immunology · 2023Article
- Genetic and Diet-Induced Animal Models for Non-Alcoholic Fatty Liver Disease (NAFLD) Research.International journal of molecular sciences · 2022Review
- Polyploidization of Hepatocytes: Insights into the Pathogenesis of Liver Diseases.Biomolecules & therapeutics · 2022Review
- Guizhi Fuling pill attenuates liver fibrosisBioengineered · 2022Article
- Matrix stiffness and shear stresses modulate hepatocyte functions in a fibrotic liver sinusoidal model.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- Liver Injury Increases the Incidence of HCC following AAV Gene Therapy in Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Small Molecule Cjoc42 Improves Chemo-Sensitivity and Increases Levels of Tumor Suppressor Proteins in Hepatoblastoma Cells and in Mice by Inhibiting Oncogene Gankyrin.Frontiers in pharmacology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Nonalcoholic fatty liver disease (NAFLD) involves development of hepatic steatosis, fibrosis, and steatohepatitis. Because hepatic steatosis appears first in NAFLD animal models, the current therapy development focuses on inhibition of hepatic steatosis, suggesting that further steps of NAFLD will be also inhibited. In this report, we show that the first event of NAFLD is liver proliferation, which drives fibrosis in NAFLD. We have deleted a strong driver of liver proliferation, gankyrin (Gank), and examined development of NAFLD in this animal model under conditions of a high-fat diet (HFD). We found that proliferating livers of wild-type mice develop fibrosis; however, livers of Gank liver-specific knockout (GLKO) mice with reduced proliferation show no fibrosis. Interestingly, an HFD causes the development of strong macrovesicular steatosis in GLKO mice and is surprisingly associated with improvements in animal health. We observed that key regulators of liver biology CCAAT/enhancer binding protein α (C/EBPα), hepatocyte nuclear factor 4α (HNF4α), p53, and CUG repeat binding protein 1 (CUGBP1) are elevated due to the deletion of Gank and that these proteins support liver functions leading to healthy conditions in GLKO mice under an HFD. To examine the role of one of these proteins in the protection of liver from fibrosis, we used CUGBP1-S302A knockin mice, which have a reduction of CUGBP1 due to increased degradation of this mutant by Gank. These studies show that reduction of CUGBP1 inhibits steatosis and facilitates liver proliferation, leading to fibrosis and the development of liver tumors.
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.