ArticleJHEP reports : innovation in hepatology2023
Spatial molecular and cellular determinants of STAT3 activation in liver fibrosis progression in non-alcoholic fatty liver disease.
Article in JHEP reports : innovation in hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 39 citations in OpenAlex.
- ADAMTS4 elicits myeloid-derived immune cell recruitment and liver fibrogenesis in metabolic dysfunction-associated steatotic liver disease.Signal transduction and targeted therapy · 2026Article
- Chemoproteomics identifies STAT3 as a key target of baicalin in ameliorating liver fibrosis.National science review · 2026Article
- A bio-fortified whole tomato food supplement as potential dietary tool for the management of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Journal of translational medicine · 2026Article
- Hepatogenomics of MAFLD in Asian Population: Genetic Polymorphisms and Pathway-Based Insights.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- BRUCE liver-KO enhances MASLD/MASH development in the steatotic PTEN-KO background by impairing mitochondrial metabolism and activating STAT3.Cell death & disease · 2025Article
- Digital pathology and spatial omics in steatohepatitis: Clinical applications and discovery potentials.Hepatology (Baltimore, Md.) · 2025Review
- Diammonium Glycyrrhizinate Alleviated Myocardial Fibrosis Induced by Isoprenaline Via Modulation of STAT/Smad3 Pathway.Journal of cardiovascular translational research · 2025Article
- A non-apoptotic caspase-8-meteorin pathway in hepatocytes promotes MASH fibrosis.Nature metabolism · 2025Article
- Orchestration of Gut-Liver-Associated Transcription Factors in MAFLD: From Cross-Organ Interactions to Therapeutic Innovation.Biomedicines · 2025Review
- Integrating Molecular Testing With Clinical Criteria and Histopathology Improves Diagnostic Precision in Immune-Mediated Liver Diseases.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2025Article
- Gout drives metabolic dysfunction-associated steatotic liver disease through gut microbiota and inflammatory mediators.Scientific reports · 2025Article
- Phase I Trial of TTI-101, a First-in-Class Oral Inhibitor of STAT3, in Patients with Advanced Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Clusterin inhibits lipopolysaccharide induced liver injury.Scientific reports · 2025Article
- Organoids for Obesity-related Diseases: Disease Models and Drug Screening.Current stem cell research & therapy · 2025Review
- Elongation factor 1A1 inhibition elicits changes in lipid droplet size, the bulk transcriptome, and cell type-associated gene expression in MASLD mouse liver.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Targeting C21orf58 is a Novel Treatment Strategy of Hepatocellular Carcinoma by Disrupting the Formation of JAK2/C21orf58/STAT3 Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Perilipin 5 deletion protects against nonalcoholic fatty liver disease and hepatocellular carcinoma by modulating lipid metabolism and inflammatory responses.Cell death discovery · 2024Article
- ASGR1 deficiency diverts lipids toward adipose tissue but results in liver damage during obesity.Cardiovascular diabetology · 2024Article
- Synergistic Differential DNA Demethylation Activity ofBiomedicines · 2024Article
- Phosphatidic acid-enabled MKL1 contributes to liver regeneration: Translational implication in liver failure.Acta pharmaceutica Sinica. B · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Background & Aims: The prevalence of non-alcoholic fatty liver disease (NAFLD) and its severe form, non-alcoholic steatohepatitis (NASH), is increasing. Individuals with NASH often develop liver fibrosis and advanced liver fibrosis is the main determinant of mortality in individuals with NASH. We and others have reported that STAT3 contributes to liver fibrosis and hepatocellular carcinoma in mice. Methods: Here, we explored whether STAT3 activation in hepatocyte and non-hepatocyte areas, measured by phospho-STAT3 (pSTAT3), is associated with liver fibrosis progression in 133 patients with NAFLD. We further characterized the molecular and cellular determinants of STAT3 activation by integrating spatial distribution and transcriptomic changes in fibrotic NAFLD livers.Results: pSTAT3 scores in non-hepatocyte areas progressively increased with fibrosis severity (r = 0.53, Conclusion: Increased understanding of the spatial dependence of STAT3 signaling in NASH and liver fibrosis progression could lead to novel targeted treatment approaches. Impact and implications: Advanced liver fibrosis is the main determinant of mortality in patients with NASH. This study showed using liver biopsies from 133 patients with NAFLD, that STAT3 activation in non-hepatocyte areas is strongly associated with fibrosis severity, inflammation, and progression to NASH. STAT3 activation was enriched in hepatic progenitor cells (HPCs) and sinusoidal endothelial cells (SECs), as determined by innovative technologies interrogating the spatial distribution of pSTAT3. Finally, STAT3 inhibition in mice resulted in reduced liver fibrosis and depletion of HPCs, suggesting that STAT3 activation in HPCs contributes to their expansion and fibrogenesis in NAFLD.
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.