ArticleOncotarget2015
LPS-induced TNF-α factor mediates pro-inflammatory and pro-fibrogenic pattern in non-alcoholic fatty liver disease.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.
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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
62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 144 citations in OpenAlex.
- Probiotics as emerging adjuncts in metabolic associated fatty liver disease therapy-a systemic review.BMC gastroenterology · 2026Pooled it
- Association of Inflammatory Cytokines With Non-Alcoholic Fatty Liver Disease.Frontiers in immunology · 2022Pooled it
- Misoprostol for non-alcoholic steatohepatitis: a randomised control trial.BMJ open gastroenterology · 2024Trial
- Dual GIP/GLP-1 receptor agonist tirzepatide ameliorates hepatic steatosis and inflammatory responses in a MASLD mouse model associated with the CCL2/CCR2 axis.BMC gastroenterology · 2026Article
- Gut Microbiota, Diet and Lipid Metabolism in Adolescents with NAFLD and Their Role in Preventive Strategies.International journal of molecular sciences · 2026Review
- Senescent hepatic stellate cells drive inflammation and disease progression in MASH (Review).Experimental and therapeutic medicine · 2026Review
- [Research progress on the multidimensional regulation of gut microbiota on metabolism, immunity, and inflammatory response in metabolic associated fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Proteomic Profiling of Alveolar Macrophages Identifies Loss of Lysosomal Content as an Indicator of Nanofiber-Induced Frustrated Phagocytosis.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Increased intestinal permeability and bile acid accumulation via inhibition of the FXR-SHP pathway contribute to coumarin-induced systemic inflammation.Microbiology spectrum · 2025Article
- Intravenously injected poly(amino acid) nanoformulation relieves spinal cord injury through synergistical modulation of microenvironments.Materials today. Bio · 2025Article
- Bile acid metabolism and signaling in health and disease: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Article
- Glucose inhibits the inflammatory response in goose fatty liver by increasing the ubiquitination level of PKA.Journal of animal science · 2024Article
- Endotoxemia and Gastrointestinal Cancers: Insight into the Mechanisms Underlying a Dangerous Relationship.Microorganisms · 2023Review
- Diclofenac Disrupts the Circadian Clock and through Complex Cross-Talks Aggravates Immune-Mediated Liver Injury-A Repeated Dose Study in Minipigs for 28 Days.International journal of molecular sciences · 2023Article
- Feeding soy protein concentrates with low or high isoflavone decreases liver inflammation by reducing lipopolysaccharide translocation.Frontiers in nutrition · 2023Article
- Network Pharmacology and Molecular Docking Study on the Multi-Target Mechanisms ofPlants (Basel, Switzerland) · 2022Article
- Gut-Liver Axis and Non-Alcoholic Fatty Liver Disease: A Vicious Circle of Dysfunctions Orchestrated by the Gut Microbiome.Biology · 2022Review
- Combination Treatment with Hydroxytyrosol and Vitamin E Improves NAFLD-Related Fibrosis.Nutrients · 2022Article
- Annexin A2 (ANXA2) regulates the transcription and alternative splicing of inflammatory genes in renal tubular epithelial cells.BMC genomics · 2022Article
2 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
17 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharide (LPS) is currently considered one of the major players in non-alcoholic fatty liver disease (NAFLD) pathogenesis and progression. Here, we aim to investigate the possible role of LPS-induced TNF-α factor (LITAF) in inducing a pro-inflammatory and pro-fibrogenic phenotype of non-alcoholic steatohepatitis (NASH).We found that children with NAFLD displayed, in different liver-resident cells, an increased expression of LITAF which correlated with histological traits of hepatic inflammation and fibrosis. Total and nuclear LITAF expression increased in mouse and human hepatic stellate cells (HSCs). Moreover, LPS induced LITAF-dependent transcription of IL-1β, IL-6 and TNF-α in the clonal myofibroblastic HSC LX-2 cell line, and this effect was hampered by LITAF silencing. We showed, for the first time in HSCs, that LITAF recruitment to these cytokine promoters is LPS dependent. However, preventing LITAF nuclear translocation by p38MAPK inhibitor, the expression of IL-6 and TNF-α was significantly reduced with the aid of p65NF-ĸB, while IL-1β transcription exclusively required LITAF expression/activity. Finally, IL-1β levels in plasma mirrored those in the liver and correlated with LPS levels and LITAF-positive HSCs in children with NASH.In conclusion, a more severe histological profile in paediatric NAFLD is associated with LITAF over-expression in HSCs, which in turn correlates with hepatic and circulating IL-1β levels outlining a panel of potential biomarkers of NASH-related liver damage. The in vitro study highlights the role of LITAF as a key regulator of the LPS-induced pro-inflammatory pattern in HSCs and suggests p38MAPK inhibitors as a possible therapeutic approach against hepatic inflammation in NASH.
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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.