ReviewCellular and molecular life sciences : CMLS2018
Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease.
Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 772 papers, 5 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
772 citing papers in PubMed, 5 syntheses or guidelines pooled it, 1,394 citations in OpenAlex.
- Association between metabolic dysfunction-associated steatotic liver disease/non-alcoholic fatty liver disease and chronic kidney disease: a systematic review and meta-analysis.Reviews in endocrine & metabolic disorders · 2026Pooled it
- Serum lipid alterations in oral squamous cell carcinoma and oral potentially malignant disorders: A systematic review and meta-analysis.Scientific reports · 2026Pooled it
- Mapping GLP-1 receptor agonist research across the MASLD-MASH-HCC continuum: a bibliometric and translational analysis.Frontiers in medicine · 2026Pooled it
- Mapping the global research output of Traditional Chinese Medicine in the treatment of metabolic dysfunction-associated steatotic liver disease: a comprehensive bibliometric analysis based on multiple databases (2000-2025).Frontiers in medicine · 2026Pooled it
- The diagnostic value of MRI-PDFF in hepatic steatosis of patients with metabolic dysfunction-associated steatotic liver disease: a systematic review and meta-analysis.BMC gastroenterology · 2025Pooled it
- Metabolomic signatures of hepatic steatosis reveal heterogeneity in cardiometabolic risk and responses to lifestyle interventions in type 2 diabetes: a post hoc analysis.Cardiovascular diabetology · 2026Trial
- Divergent Hypoxia-Inducible Factor 2‑Alpha Signaling in Alcoholic Liver Disease and Metabolic Dysfunction-Associated Steatotic Liver Disease.ACS pharmacology & translational science · 2026Review
- Apigenin attenuates MASLD progression by suppressing lipogenesis and macrophage M1-like inflammatory activation: involvement of SMAD4-associated signaling.Journal of molecular histology · 2026Article
- Stearoyl CoA desaturase 1 deficiency increases ferroptosis susceptibility in chicken embryonic liver cells.Poultry science · 2026Article
- DDX3X overexpression in mice can cause rapid tissue-specific toxicity and mortality.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Flavonoids for MASLD: Hepatic Lipid Targets, Biopharmaceutic Barriers, and Formulation Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Acute and 28-Day Toxicity Evaluation of New Pleuromutilin Derivative 4g.Journal of applied toxicology : JAT · 2026Article
- Article
- Mitophagy and Noncoding RNA Regulation in Type 2 Diabetes Mellitus: Molecular Mechanisms, Tissue-Specific Evidence and Translational Perspective.Biomedicines · 2026Review
- Lutein Attenuates Lipid Accumulation in Association with TFEB Nuclear Translocation and Autophagy-Lysosomal Responses in a Cellular Model of Hepatic Steatosis.Antioxidants (Basel, Switzerland) · 2026Article
- Low-Dose, Long-TermInternational journal of molecular sciences · 2026Article
- Article
- Article
- MASLD: Spatial Mechanisms and New Therapeutics.Biomolecules · 2026Review
- Potential Targets in Nonalcoholic Steatohepatitis Based on Bioinformatics Analysis and Machine Learning Strategies.Biochemical genetics · 2026Article
712 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is currently the world's most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases.
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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.