ReviewMammalian genome : official journal of the International Mammalian Genome Society2014
Modeling progressive non-alcoholic fatty liver disease in the laboratory mouse.
Review in Mammalian genome : official journal of the International Mammalian Genome Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
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Who cites it
21 citing papers in PubMed.
- Non-alcoholic fatty liver disease: pathogenesis and models.American journal of translational research · 2024Review
- Treatment of rheumatoid arthritis with conventional, targeted and biological disease-modifying antirheumatic drugs in the setting of liver injury and non-alcoholic fatty liver disease.Rheumatology international · 2022Review
- Liver fibrosis: Pathophysiology and clinical implications.WIREs mechanisms of disease · 2021Review
- Dysregulation of bile acids increases the risk for preterm birth in pregnant women.Nature communications · 2020Article
- Integrative analysis of blood and gut microbiota data suggests a non-alcoholic fatty liver disease (NAFLD)-related disorder in French SLAScientific reports · 2020Article
- Review
- A new method to induce nonalcoholic steatohepatitis (NASH) in mice.BMC gastroenterology · 2019Article
- The FATZO mouse, a next generation model of type 2 diabetes, develops NAFLD and NASH when fed a Western diet supplemented with fructose.BMC gastroenterology · 2019Article
- Effects of high fat medium conditions on cellular gene expression profile: a network analysis approach.Gastroenterology and hepatology from bed to bench · 2019Article
- n-3 PUFAs reduce tumor load and improve survival in a NASH-tumor mouse model.Therapeutic advances in chronic disease · 2019Article
- Bioinformatics Analysis of Key Differentially Expressed Genes in Nonalcoholic Fatty Liver Disease Mice Models.Gene expression · 2018Article
- Updates on Dietary Models of Nonalcoholic Fatty Liver Disease: Current Studies and Insights.Gene expression · 2018Review
- Ghrelin deletion protects against age-associated hepatic steatosis by downregulating the C/EBPα-p300/DGAT1 pathway.Aging cell · 2018Article
- Protective Effect of Meretrix meretrix Oligopeptides on High-Fat-Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice.Marine drugs · 2018Article
- Microcirculatory disturbances and cellular changes during progression of hepatic steatosis to liver tumors.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- Article
- A systems biology analysis protein-protein interaction of NASH and IBD based on comprehensive gene information.Gastroenterology and hepatology from bed to bench · 2017Article
- Hepatic Deletion of Janus Kinase 2 Counteracts Oxidative Stress in Mice.Scientific reports · 2016Article
- The kielin/chordin-like protein KCP attenuates nonalcoholic fatty liver disease in mice.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- How Useful Are Monogenic Rodent Models for the Study of Human Non-Alcoholic Fatty Liver Disease?Frontiers in endocrinology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in the world and its prevalence is rising. In the absence of disease progression, fatty liver poses minimal risk of detrimental health outcomes. However, advancement to non-alcoholic steatohepatitis (NASH) confers a markedly increased likelihood of developing severe liver pathologies, including fibrosis, cirrhosis, organ failure, and cancer. Although a substantial percentage of NAFLD patients develop NASH, the genetic and molecular mechanisms driving this progression are poorly understood, making it difficult to predict which patients will ultimately develop advanced liver disease. Deficiencies in mechanistic understanding preclude the identification of beneficial prognostic indicators and the development of effective therapies. Mouse models of progressive NAFLD serve as a complementary approach to the direct analysis of human patients. By providing an easily manipulated experimental system that can be rigorously controlled, they facilitate an improved understanding of disease development and progression. In this review, we discuss genetically- and chemically-induced models of NAFLD that progress to NASH, fibrosis, and liver cancer in the context of the major signaling pathways whose disruption has been implicated as a driving force for their development. Additionally, an overview of nutritional models of progressive NAFLD is provided.
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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.