ReviewCancers2023
NAFLD-Related HCC: Focus on the Latest Relevant Preclinical Models.
Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 16 citations in OpenAlex.
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- Dynamic AFP-Defined Disease State Transitions in Hospitalized Patients with Hepatocellular Carcinoma Using the Multi-State Markov Model: A Retrospective Cohort Study.Journal of hepatocellular carcinoma · 2026Article
- TM4SF5-mediated KEAP1 Regulation in Hepatocytes Irrelevant to NRF2 Expression and Activity Promotes Oxidative Stress and Inflammation to Develop Metabolic Dysfunction-Associated Steatotic Liver Disease.International journal of biological sciences · 2026Article
- Hydrogel-Based Immunomodulation of Tumor Immune Microenvironment in Hepatocellular Carcinoma: Current Strategies and Future Directions.International journal of nanomedicine · 2026Review
- From bioinformatics to clinical translation: BIRC5 as a pivotal diagnostic biomarker and therapeutic target for NAFLD-driven HCC.Cell biology and toxicology · 2025Article
- Cutting edge: ferroptosis in metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis and therapy.Functional & integrative genomics · 2025Review
- Rifaximin prophylaxis in MASLD‑hepatocellular carcinoma: Lessons from a negative animal model.Biomedical reports · 2025Article
- Administration of a probiotic supplement attenuates nonalcoholic fatty liver disease by reducing hepatic lipid accumulation, oxidative stress, and inflammation.Bioscience of microbiota, food and health · 2025Article
- Inflammatory Response in the Pathogenesis and Treatment of Hepatocellular Carcinoma: A Double-Edged Weapon.International journal of molecular sciences · 2024Review
- The Influence of Diet and Its Components on the Development and Prevention of Hepatocellular Carcinoma (HCC).Cancers · 2024Review
- Precision targeting in hepatocellular carcinoma: Exploring ligand-receptor mediated nanotherapy.World journal of hepatology · 2024Review
- Obesity under the moonlight of c-MYC.Frontiers in cell and developmental biology · 2023Review
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
Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and one of the deadliest cancers worldwide. Despite extensive research, the biological mechanisms underlying HCC's development and progression remain only partially understood. Chronic overeating and/or sedentary-lifestyle-associated obesity, which promote Non-Alcoholic Fatty Liver Disease (NAFLD), have recently emerged as worrying risk factors for HCC. NAFLD is characterized by excessive hepatocellular lipid accumulation (steatosis) and affects one quarter of the world's population. Steatosis progresses in the more severe inflammatory form, Non-Alcoholic Steatohepatitis (NASH), potentially leading to HCC. The incidence of NASH is expected to increase by up to 56% over the next 10 years. Better diagnoses and the establishment of effective treatments for NAFLD and HCC will require improvements in our understanding of the fundamental mechanisms of the disease's development. This review describes the pathogenesis of NAFLD and the mechanisms underlying the transition from NAFL/NASH to HCC. We also discuss a selection of appropriate preclinical models of NAFLD for research, from cellular models such as liver-on-a-chip models to in vivo models, focusing particularly on mouse models of dietary NAFLD-HCC.
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.