ArticleCell2018
Obesity Drives STAT-1-Dependent NASH and STAT-3-Dependent HCC.
Article in Cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 241 papers.
What it found
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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
241 citing papers in PubMed, 353 citations in OpenAlex.
- Normal weight, hidden risk: adiposity is a better determinant of liver cancer than body mass index.Hepatobiliary surgery and nutrition · 2026Article
- LGR5-positive fibroblasts orchestrate skin mechanoadaptation through JAK1 modulation.Nature communications · 2026Article
- Molecular mechanisms and pathogenesis of MASH.Nature · 2026Review
- Revisiting cannabinoid receptor-2: a key regulator of hepatic steatosis, inflammatory cascades, and fibrotic progression.Archives of toxicology · 2026Review
- Molecular Mechanisms and Targeted Therapies of PTPN2 in Metabolic Diseases: A Review.Biomolecules · 2026Review
- Hepatic glutathione depletion ameliorates MASLD through selective protein oxidation and inhibition of lipogenesis.The Journal of clinical investigation · 2026Article
- SOCS1-based therapeutic peptides improve liver disease and metabolic dysfunction in obesity and diabetes.Scientific reports · 2026Article
- Senescent hepatic stellate cells drive inflammation and disease progression in MASH (Review).Experimental and therapeutic medicine · 2026Review
- Targeting STE20-type kinase MST3 improves metabolic dysfunction-associated steatohepatitis without affecting hepatocellular carcinoma development in mice.BMC medicine · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Mechanisms, functions and therapeutic targeting of protein tyrosine phosphatases.Nature reviews. Molecular cell biology · 2026Review
- Identification of the E3 ligase TRIM21 as a crucial regulator of STAT1 in metabolic dysfunction-associated steatohepatitis.Cell communication and signaling : CCS · 2026Article
- Comparative study of obeticholic acid and rosuvastatin in high-fat/fructose diet-induced metabolic dysfunction: role of AMPK, PPAR-γ, SREBP-1c, and STAT3 pathways.Journal of molecular histology · 2026Article
- Repurposing Resmetirom suppresses MASH-associated hepatocellular carcinoma, with mechanistic implications of MDK/LRP1-mediated metabolic reprogramming and immunosuppression.Hepatology (Baltimore, Md.) · 2026Article
- Macrophage-linked lipid metabolic signatures for HCC prognosis identified through integrated bulk and single-cell transcriptomics.Frontiers in immunology · 2026Article
- Integrated Bioinformatics Analysis Revealing that the NSDHL Gene Might Be Associated with the Progression of Western HFD/SW-Induced Hepatocellular CarcinomaEndocrine, metabolic & immune disorders drug targets · 2026Article
- Targeting PKLR and lipogenic enzymes through JNK inhibition to develop a therapeutic strategy for MASLD and MASH.Frontiers in pharmacology · 2026Article
- The impact of chronic comorbidities on cancer immunoediting: challenges and opportunities for immunotherapies.Frontiers in immunology · 2026Review
- Deoxycholic Acid and Lipoteichoic Acid cooperatively drive macrophage M2/M1 polarization via TGR5/STAT3 and TLR2/NF-κB to fuel HCC progression in obesity.Metabolism open · 2025Article
- Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025Review
181 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
Obesity is a major driver of cancer, especially hepatocellular carcinoma (HCC). The prevailing view is that non-alcoholic steatohepatitis (NASH) and fibrosis or cirrhosis are required for HCC in obesity. Here, we report that NASH and fibrosis and HCC in obesity can be dissociated. We show that the oxidative hepatic environment in obesity inactivates the STAT-1 and STAT-3 phosphatase T cell protein tyrosine phosphatase (TCPTP) and increases STAT-1 and STAT-3 signaling. TCPTP deletion in hepatocytes promoted T cell recruitment and ensuing NASH and fibrosis as well as HCC in obese C57BL/6 mice that normally do not develop NASH and fibrosis or HCC. Attenuating the enhanced STAT-1 signaling prevented T cell recruitment and NASH and fibrosis but did not prevent HCC. By contrast, correcting STAT-3 signaling prevented HCC without affecting NASH and fibrosis. TCPTP-deletion in hepatocytes also markedly accelerated HCC in mice treated with a chemical carcinogen that promotes HCC without NASH and fibrosis. Our studies reveal how obesity-associated hepatic oxidative stress can independently contribute to the pathogenesis of NASH, fibrosis, and HCC.
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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.