ReviewHepatology (Baltimore, Md.)2020
Genetic Pathways in Nonalcoholic Fatty Liver Disease: Insights From Systems Biology.
Review in Hepatology (Baltimore, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 3 of them syntheses that pooled it.
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
71 citing papers in PubMed, 3 syntheses or guidelines pooled it, 127 citations in OpenAlex.
- Efficacy and safety of GLP-1 receptor agonists in patients with metabolic-associated fatty liver diseases: an umbrella review.Frontiers in medicine · 2026Pooled it
- Vitamin E for people with non-alcoholic fatty liver disease.The Cochrane database of systematic reviews · 2024Pooled it
- rs641738C>T near MBOAT7 is associated with liver fat, ALT and fibrosis in NAFLD: A meta-analysis.Journal of hepatology · 2021Pooled it
- Excessive EFHD1-dependent ER-mitochondrial contacts drive a maladaptive antiviral response in metabolic liver disease.The Journal of clinical investigation · 2026Article
- Nutriomic Technologies for Characterizing, Diagnosing, Clustering and Managing Chronic Liver Diseases: Precision Nutrition Implications.International journal of molecular sciences · 2026Review
- Longitudinal Examination of the UA/HDL-C Ratio as a Biomarker for Fatty Liver Disease: Findings from a Five-Year Follow-Up. Genetics of Atherosclerotic Disease (GEA) Study.Diagnostics (Basel, Switzerland) · 2026Article
- Excessive CabioRxiv : the preprint server for biology · 2026Article
- Panomics in metabolic dysfunction-associated steatotic liver disease: unravelling the drivers of disease heterogeneity.Clinical and molecular hepatology · 2026Review
- Metabolic Dysfunction-associated Steatotic Liver Disease Alters Fatty Acid Profiles in the Liver and Adipose Tissue.The Journal of clinical endocrinology and metabolism · 2025Article
- The pathophysiological role of portal hypertension in metabolic dysfunction-associated steatotic liver disease.Hepatology communications · 2025Review
- Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Mechanisms, Clinical Implications and Therapeutic Advances.Endocrinology, diabetes & metabolism · 2025Review
- Deep Learning Reveals Liver MRI Features Associated With PNPLA3 I148M in Steatotic Liver Disease.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- Nutrient-Induced Changes of Liver Fat Content in Humans.Physiological research · 2025Review
- From Childhood Obesity to Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and Hyperlipidemia Through Oxidative Stress During Childhood.Metabolites · 2025Review
- ACSS2 and metabolic diseases: from lipid metabolism to therapeutic target.Lipids in health and disease · 2025Review
- Impact of Weight Loss on Metabolic Dysfunction Associated Steatohepatitis and Hepatic Fibrosis.Current diabetes reports · 2025Review
- Precision medicine and nucleotide-based therapeutics to treat steatotic liver disease.Clinical and molecular hepatology · 2025Review
- Integrated Multi-Omic Analysis Reveals Causal Relationships and Causal Mechanisms of Peripheral Lymphocyte-Driven Remodeling in the Intrahepatic Immune Microenvironment of Early-Stage MAFLD.Journal of inflammation research · 2025Article
- Silybin A fromTheranostics · 2025Article
- Genomic Exploration of Nonalcoholic Fatty Liver Disease: Insights From Gene Expression and Variation in Morbidly Obese Individuals.Journal of obesity · 2025Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning worldwide epidemic whose etiology reflects multiple interactions between environmental and genetic factors. Here, we review the major pathways and dominant genetic modifiers known to be relevant players in human NAFLD and which may determine key components of the heritability of distinctive disease traits including steatosis and fibrosis. In addition, we have employed general assumptions which are based on known genetic factors in NAFLD to build a systems biology prediction model that includes functional enrichment. This prediction model highlights additional complementary pathways that represent plausible intersecting signaling networks that we define here as an NAFLD-Reactome. We review the evidence connecting variants in each of the major known genetic modifiers (variants in patatin-like phospholipase domain containing 3, transmembrane 6 superfamily member 2, membrane-bound O-acyltransferase domain containing 7, glucokinase regulator, and hydroxysteroid 17-beta dehydrogenase 13) to NAFLD and expand the associated underlying mechanisms using functional enrichment predictions, based on both preclinical and cell-based experimental findings. These major candidate gene variants function in distinct pathways, including substrate delivery for de novo lipogenesis; mitochondrial energy use; lipid droplet assembly, lipolytic catabolism, and fatty acid compartmentalization; and very low-density lipoprotein assembly and secretion. The NAFLD-Reactome model expands these pathways and allows for hypothesis testing, as well as serving as a discovery platform for druggable targets across multiple pathways that promote NAFLD development and influence several progressive outcomes. In conclusion, we summarize the strengths and weaknesses of studies implicating selected variants in the pathophysiology of NAFLD and highlight opportunities for future clinical research and pharmacologic intervention, as well as the implications for clinical practice.
Indexed as
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.