ArticleHepatology (Baltimore, Md.)2018
The Genetic Architecture of Diet-Induced Hepatic Fibrosis in Mice.
Article in Hepatology (Baltimore, Md.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Pooled it
- p21Nature aging · 2026Article
- RUNX1-mediated repression of miR-24 promotes hepatic stellate cell activation and liver fibrosis by targeting the ALK4/Smad3 signaling pathway.Frontiers in genetics · 2026Article
- Fecal microbiota transplantation alleviates steatosis and inflammation in high-fat and high-sugar diet-induced fatty liver in mice.Frontiers in cell and developmental biology · 2026Article
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- Decoding the Liver-Heart Axis in Cardiometabolic Diseases.Circulation research · 2025Review
- Systems genetics uncovers associations among host amylase locus, gut microbiome, and metabolic traits in mice.Microbiome · 2025Article
- Functional compartmentalization of hepatic mitochondrial subpopulations during MASH progression.Communications biology · 2025Article
- Mouse Models for the Study of Liver Fibrosis RegressionJournal of clinical and translational hepatology · 2024Review
- Identification of TACSTD2 as novel therapeutic targets for cisplatin-induced acute kidney injury by multi-omics data integration.Human genetics · 2024Article
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- Review
- Hepatokine ITIH3 protects against hepatic steatosis by downregulating mitochondrial bioenergetics andiScience · 2024Article
- Systems genetics approaches for understanding complex traits with relevance for human disease.eLife · 2023Review
- Mechanisms Behind NAFLD: a System Genetics Perspective.Current atherosclerosis reports · 2023Review
- Found in translation-Fibrosis in metabolic dysfunction-associated steatohepatitis (MASH).Science translational medicine · 2023Review
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- Article
- Mouse strain-dependent variation in metabolic associated fatty liver disease (MAFLD): a comprehensive resource tool for pre-clinical studies.Scientific reports · 2023Article
- Article
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
Abstract
We report the genetic analysis of a "humanized" hyperlipidemic mouse model for progressive nonalcoholic steatohepatitis (NASH) and fibrosis. Mice carrying transgenes for human apolipoprotein E*3-Leiden and cholesteryl ester transfer protein and fed a "Western" diet were studied on the genetic backgrounds of over 100 inbred mouse strains. The mice developed hepatic inflammation and fibrosis that was highly dependent on genetic background, with vast differences in the degree of fibrosis. Histological analysis showed features characteristic of human NASH, including macrovesicular steatosis, hepatocellular ballooning, inflammatory foci, and pericellular collagen deposition. Time course experiments indicated that while hepatic triglyceride levels increased steadily on the diet, hepatic fibrosis occurred at about 12 weeks. We found that the genetic variation predisposing to NASH and fibrosis differs markedly from that predisposing to simple steatosis, consistent with a multistep model in which distinct genetic factors are involved. Moreover, genome-wide association identified distinct genetic loci contributing to steatosis and NASH. Finally, we used hepatic expression data from the mouse panel and from 68 bariatric surgery patients with normal liver, steatosis, or NASH to identify enriched biological pathways. Conclusion: The pathways showed substantial overlap between our mouse model and the human disease.
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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.