ReviewBiomedicines2023
Gene Variants Implicated in Steatotic Liver Disease: Opportunities for Diagnostics and Therapeutics.
Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- Loss of immunometabolic adaptability in MASH: gut-derived signals drive macrophage reprogramming and fibrosis.Frontiers in immunology · 2026Review
- Metabolic Dysfunction-Associated Steatotic Liver Disease: A Silent Driver of Cardiovascular Risk and a New Target for Intervention.International journal of molecular sciences · 2025Review
- Targeting CIDEB alleviates liver steatosis and fibrosis in mouse MASH models.Molecular therapy. Nucleic acids · 2025Article
- Liver-Kidney Crosstalk in Major Pediatric Diseases: Unraveling the Complexities and Clinical Challenges.Journal of clinical medicine · 2025Review
- Innovative Strategies in the Diagnosis and Treatment of Liver Cirrhosis and Associated Syndromes.Life (Basel, Switzerland) · 2025Review
- Role of PNPLA3 in Hepatic Stellate Cells and Hepatic Cellular Crosstalk.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- Precision medicine and nucleotide-based therapeutics to treat steatotic liver disease.Clinical and molecular hepatology · 2025Review
- MAFLD: A Comprehensive Review of the Link Between Metabolic Dysfunction and Cardiovascular Risk.Hepatic medicine : evidence and research · 2025Review
- Impact of genotyping (Frontiers in endocrinology · 2025Article
- Transcriptome-Wide Association Study of Metabolic Dysfunction-Associated Steatotic Liver Disease Identifies Relevant Gene Signatures.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024Article
- Metabolic dysfunction-associated steatotic liver disease and cardiovascular risk: a comprehensive review.Cardiovascular diabetology · 2024Review
- Team players in the pathogenesis of metabolic dysfunctions-associated steatotic liver disease: The basis of development of pharmacotherapy.World journal of gastrointestinal pathophysiology · 2024Review
- Fibrosis and Hepatocarcinogenesis: Role of Gene-Environment Interactions in Liver Disease Progression.International journal of molecular sciences · 2024Review
- PINK1/Park2-Mediated Mitophagy Relieve Non-Alcoholic Fatty Liver Disease.Physiological research · 2024Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD) describes a steatotic (or fatty) liver occurring as a consequence of a combination of metabolic, environmental, and genetic factors, in the absence of significant alcohol consumption and other liver diseases. NAFLD is a spectrum of conditions. Steatosis in the absence of inflammation is relatively benign, but the disease can progress into more severe forms like non-alcoholic steatohepatitis (NASH), liver cirrhosis, and hepatocellular carcinoma. NAFLD onset and progression are complex, as it is affected by many risk factors. The interaction between genetic predisposition and other factors partially explains the large variability of NAFLD phenotype and natural history. Numerous genes and variants have been identified through large-scale genome-wide association studies (GWAS) that are associated with NAFLD and one or more subtypes of the disease. Among them, the largest effect size and most consistent association have been patatin-like phospholipase domain-containing protein 3 (
Indexed as
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.