ReviewMetabolites2020
Transcriptional Regulation in Non-Alcoholic Fatty Liver Disease.
Review in Metabolites, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 49 citations in OpenAlex.
- A Modular Liver-Microbial Microfluidic Platform to Evaluate Therapeutic and Adverse Effects of Microbial Metabolites.Advanced healthcare materials · 2026Article
- Experimental Models of Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comparative Analysis of a Choline-Deficient and Cholesterol-Enriched Diet in Rats.International journal of molecular sciences · 2026Article
- A novel C/EBPα-miR-335-5p-PRKAA2 regulatory axis drives hepatic lipid accumulation in MASLD.Scientific reports · 2026Article
- Zebrafish model of palmitic acid induced MAFLD recapitulates pathways conserved in mice and humans.Scientific reports · 2025Article
- Gradual DNA methylation changes reveal transcription factors implicated in metabolic dysfunction-associated steatotic liver disease progression and epigenetic age acceleration.Clinical epigenetics · 2025Article
- Review
- FrozONE: quick cell nucleus enrichment for comprehensive proteomics analysis of frozen tissues.Life science alliance · 2025Article
- Night shift-induced circadian disruption: links to initiation of non-alcoholic fatty liver disease/non-alcoholic steatohepatitis and risk of hepatic cancer.Hepatoma research · 2024Article
- Fibrosis and Hepatocarcinogenesis: Role of Gene-Environment Interactions in Liver Disease Progression.International journal of molecular sciences · 2024Review
- Dramatic Suppression of Lipogenesis and No Increase in Beta-Oxidation Gene Expression Are among the Key Effects of Bergamot Flavonoids in Fatty Liver Disease.Antioxidants (Basel, Switzerland) · 2024Article
- E4bp4-Cyp3a11 axis in high-fat diet-induced obese mice with weight fluctuation.Nutrition & metabolism · 2024Article
- Changes in Macronutrients during Dieting Lead to Weight Cycling and Metabolic Complications in Mouse Model.Nutrients · 2024Article
- Genistein and Sex Hormone Supplementation Modulated Hepatic PPARα, δ, and γ Subtypes and STAT1 Expressions in a NASH Rat Model with Bilateral Orchidectomy.Biomedicines · 2024Article
- Hepatocyte FBXW7-dependent activity of nutrient-sensing nuclear receptors controls systemic energy homeostasis and NASH progression in male mice.Nature communications · 2023Article
- Circadian rhythms and inflammatory diseases of the liver and gut.Liver research (Beijing, China) · 2023Review
- The interplay between dietary fatty acids and gut microbiota influences host metabolism and hepatic steatosis.Nature communications · 2023Article
- LY6D is crucial for lipid accumulation and inflammation in nonalcoholic fatty liver disease.Experimental & molecular medicine · 2023Article
- Specificity Proteins (SP) and Krüppel-like Factors (KLF) in Liver Physiology and Pathology.International journal of molecular sciences · 2023Review
- The Role of the NLRP3 Inflammasome and Programmed Cell Death in Acute Liver Injury.International journal of molecular sciences · 2023Review
- Positive allosteric GABAFrontiers in physiology · 2023Article
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
Obesity is the primary risk factor for the pathogenesis of non-alcoholic fatty liver disease (NAFLD), the worldwide prevalence of which continues to increase dramatically. The liver plays a pivotal role in the maintenance of whole-body lipid and glucose homeostasis. This is mainly mediated by the transcriptional activation of hepatic pathways that promote glucose and lipid production or utilization in response to the nutritional state of the body. However, in the setting of chronic excessive nutrition, the dysregulation of hepatic transcriptional machinery promotes lipid accumulation, inflammation, metabolic stress, and fibrosis, which culminate in NAFLD. In this review, we provide our current understanding of the transcription factors that have been linked to the pathogenesis and progression of NAFLD. Using publicly available transcriptomic data, we outline the altered activity of transcription factors among humans with NAFLD. By expanding this analysis to common experimental mouse models of NAFLD, we outline the relevance of mouse models to the human pathophysiology at the transcriptional level.
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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.