ArticleJournal of biomedical research2018
Non-alcoholic fatty liver disease: a narrative review of genetics.
Article in Journal of biomedical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 46 citations in OpenAlex.
- Causal Effects of a Hepatic Senescence Gene Set on MASLD Fibrosis: A Mendelian Randomization Study and Quercetin Molecular Docking Analysis.Biomedicines · 2026Article
- Hypoxia-inducible factors in the immunometabolism of metabolic dysfunction-associated steatotic liver disease (MASLD): molecular mechanisms and therapeutic implications.Frontiers in physiology · 2026Article
- Nutritional and Fasting Strategies for the Management of MASLD/MASH: An Integrative Review.JGH open : an open access journal of gastroenterology and hepatology · 2025Review
- IREB2 Knockdown Alleviates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease by TLR4/NF-κB Signaling Inactivation.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- Metabolic and genetic mechanisms of metabolic dysfunction-associated steatotic liver disease: an integrative perspective from molecular pathways to clinical challenges.Frontiers in endocrinology · 2025Review
- Synergistic Differential DNA Demethylation Activity ofBiomedicines · 2024Article
- Advances in Noninvasive Biomarkers for Nonalcoholic Fatty Liver Disease.Metabolites · 2023Review
- Dnmt1/Tet2-mediated changes in Cmip methylation regulate the development of nonalcoholic fatty liver disease by controlling the Gbp2-Pparγ-CD36 axis.Experimental & molecular medicine · 2023Article
- Plasma Metabolomic and Lipidomic Profiling of Metabolic Dysfunction-Associated Fatty Liver Disease in Humans Using an Untargeted Multiplatform Approach.Metabolites · 2022Article
- Race and Ethnicity in Non-Alcoholic Fatty Liver Disease (NAFLD): A Narrative Review.Nutrients · 2022Review
- Nonalcoholic fatty liver disease (NAFLD) from pathogenesis to treatment concepts in humans.Molecular metabolism · 2021Review
- Development of a novel machine learning model to predict presence of nonalcoholic steatohepatitis.Journal of the American Medical Informatics Association : JAMIA · 2021Article
- Human biomimetic liver microphysiology systems in drug development and precision medicine.Nature reviews. Gastroenterology & hepatology · 2021Review
- Assessment of Lifestyle Factors Helps to Identify Liver Fibrosis Due to Non-Alcoholic Fatty Liver Disease in Obesity.Nutrients · 2021Article
- Effects of TM6SF2 E167K on hepatic lipid and very low-density lipoprotein metabolism in humans.JCI insight · 2020Article
- Predicting and elucidating the etiology of fatty liver disease: A machine learning modeling and validation study in the IMI DIRECT cohorts.PLoS medicine · 2020Article
- Non-Alcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus: A Position Statement of the Fatty Liver Research Group of the Korean Diabetes Association.Diabetes & metabolism journal · 2020Review
- Noninvasive Evaluation of Nonalcoholic Fatty Liver Disease.Endocrinology and metabolism (Seoul, Korea) · 2020Review
- Differential Associations of Circulating MicroRNAs With Pathogenic Factors in NAFLD.Hepatology communications · 2020Article
- HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels.Bioscience reports · 2020Article
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is now the most common cause of chronic liver diseases worldwide. It encompasses a spectrum of disorders ranging from isolated hepatic steatosis to nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma. One of the key challenges in NAFLD is identifying which patients will progress. Epidemiological and genetic studies indicate a strong pattern of heritability that may explain some of the variability in NAFLD phenotype and risk of progression. To date, at least three common genetic variants in the PNPLA3, TM6SF2, and GCKR genes have been robustly linked to NAFLD in the population. The function of these genes revealed novel pathways implicated in both the development and progression of NAFLD. In addition, candidate genes previously implicated in NAFLD pathogenesis have also been identified as determinants or modulators of NAFLD phenotype including genes involved in hepatocellular lipid handling, insulin resistance, inflammation, and fibrogenesis. This article will review the current understanding of the genetics underpinning the development of hepatic steatosis and the progression of NASH. These newly acquired insights may transform our strategy to risk-stratify patients with NAFLD and to identify new potential therapeutic targets.
Identifiers
What Socratic 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 Socratic graph.