ReviewBiomedicines2021
Natural Progression of Non-Alcoholic Steatohepatitis to Hepatocellular Carcinoma.
Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis 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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Mechanistic insights into the pleiotropic effects of butyrate as a potential therapeutic agent on NAFLD management: A systematic review.Frontiers in nutrition · 2022Pooled it
- Bioinformatics and experimental validation of druggable targets in non-alcoholic fatty liver disease.Scientific reports · 2026Article
- Gypenoside XLIX and Mitochondria-Associated ER Membranes in Non-Alcoholic Fatty Liver Disease: Mechanistic Insights and Emerging Perspectives.Molecules (Basel, Switzerland) · 2026Review
- GNMT and Its Regulatory MicroRNAs as Biomarkers and Therapeutic Targets for Metabolic Dysfunction-Associated Fatty Liver Disease and Hepatocellular Carcinoma.International journal of molecular sciences · 2026Review
- Deficiency of β-arrestin2 ameliorates MASLD in mice by promoting the activation of TAK1/AMPK signaling.Archives of pharmacal research · 2025Article
- Therapeutic potential of kakkatin derivatives against hepatocellular carcinoma.World journal of clinical oncology · 2025Article
- Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC.International journal of molecular sciences · 2024Review
- Isoliquiritigenin in combination with visceral adipose tissue and related markers as a predictive tool for nonalcoholic fatty liver disease.Journal of physiology and biochemistry · 2024Article
- Exploring the role of genetic variations in NAFLD: implications for disease pathogenesis and precision medicine approaches.European journal of medical research · 2024Review
- Identification of Fast Progressors Among Patients With Nonalcoholic Steatohepatitis Using Machine Learning.Gastro hep advances · 2024Article
- Myo-inositol supplementation improves cardiometabolic factors, anthropometric measures, and liver function in obese patients with non-alcoholic fatty liver disease.Frontiers in nutrition · 2023Article
- Increased CHCHD2 expression promotes liver fibrosis in nonalcoholic steatohepatitis via Notch/osteopontin signaling.JCI insight · 2022Article
- NASH and Systemic Complications: From Basic to Clinical Research.Biomedicines · 2021Article
- Review
- Article
- Impaired Response to Immunotherapy in Non-Alcoholic Steatohepatitis-Related Hepatocellular Carcinoma?Liver cancer · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic steatohepatitis (NASH) is a chronic and progressive form of non-alcoholic fatty liver disease (NAFLD). Its global incidence is increasing which makes NASH an epidemic and a public health threat. Due to repeated insults to the liver, patients are at risk for developing hepatocellular carcinoma (HCC). The progression of NASH to HCC was initially defined according to a two-hit model which involved the development of steatosis, followed by lipid peroxidation and inflammation. However, current research defines a "multi-hit" or "multi-parallel hit" model which synthesizes several contributing pathways involved in progressive fibrosis and oncogenesis. This perspective considers the effects of cellular, genetic, immunologic, metabolic, and endocrine pathways leading up to HCC which underscores the complexity of this condition. This article will provide an updated review of the pathogenic mechanisms leading from NASH to HCC as well as an exploration of the role of biomarkers and screening.
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.