ArticlePloS one2010
Hepatic expression patterns of inflammatory and immune response genes associated with obesity and NASH in morbidly obese patients.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 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
142 citing papers in PubMed, 233 citations in OpenAlex.
- Interferon gamma-induced protein 10 is associated with insulin resistance and incident diabetes in patients with nonalcoholic fatty liver disease.Scientific reports · 2015Trial
- Metabolic dysfunction-associated steatohepatitis in the real world: clinical burden, disease progression, and risk stratification with non-invasive tests.BMC gastroenterology · 2026Article
- Role of central and peripheral serotonin in liver physiology and diseases.Theranostics · 2026Review
- The double-edged sword of regulatory T cells in MASLD: from inflammation control to fibrosis promotion.Animal cells and systems · 2026Review
- CXCL6 exacerbates metabolic dysfunction-associated steatohepatitis by suppressing LPIN1-mediated fatty acid oxidation in hepatocytes.International journal of biological sciences · 2026Article
- Cell Therapy in Advanced Cirrhosis: From Preclinical Evidence to Clinical Application.Gastro hep advances · 2026Review
- Dissecting the mechanisms of MASLD fibrosis in the era of single-cell and spatial omics.The Journal of clinical investigation · 2025Review
- Association of hepatic steatosis with increased plasma xanthine oxidoreductase activity: MedCity21 health examination registry.Metabolism open · 2025Article
- Inflammation in MASLD progression and cancer.JHEP reports : innovation in hepatology · 2025Review
- Hormone correction of dysfunctional metabolic gene expression in stem cell-derived liver tissue.Stem cell research & therapy · 2025Article
- Immunology and treatments of fatty liver disease.Archives of toxicology · 2025Review
- The mitochondrial TSPO ligand Atriol mitigates metabolic-associated steatohepatitis by downregulating CXCL1.Metabolism: clinical and experimental · 2024Article
- Medaka liver developed Human NAFLD-NASH transcriptional signatures in response to ancestral bisphenol A exposure.Research square · 2024Article
- The Role of CD4International journal of molecular sciences · 2024Review
- Sex-specific expression of the human NAFLD-NASH transcriptional signatures in the liver of medaka with a history of ancestral bisphenol A exposure.bioRxiv : the preprint server for biology · 2024Article
- Immune system dysregulation in the pathogenesis of non-alcoholic steatohepatitis: unveiling the critical role of T and B lymphocytes.Frontiers in immunology · 2024Review
- Acyl-CoA Thioesterase 1 Contributes to Transition of Steatosis to Metabolic-Associated Steatohepatitis.International journal of hepatology · 2024Article
- Active role of the immune system in metabolic dysfunction-associated steatotic liver disease.Gastroenterology report · 2024Review
- Associations between systemic inflammation indicators and nonalcoholic fatty liver disease: evidence from a prospective study.Frontiers in immunology · 2024Article
- The bidirectional immune crosstalk in metabolic dysfunction-associated steatotic liver disease.Cell metabolism · 2023Review
82 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
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundObesity modulates inflammation and activation of immune pathways which can lead to liver complications. We aimed at identifying expression patterns of inflammatory and immune response genes specifically associated with obesity and NASH in the liver of morbidly obese patients. METHODOLOGY/PRINCIPAL
findingsExpression of 222 genes was evaluated by quantitative RT-PCR in the liver of morbidly obese patients with histologically normal liver (n = 6), or with severe steatosis without (n = 6) or with NASH (n = 6), and in lean controls (n = 5). Hepatic expression of 58 out of 222 inflammatory and immune response genes was upregulated in NASH patients. The most notable changes occurred in genes encoding chemokines and chemokine receptors involved in leukocyte recruitment, CD and cytokines involved in the T cell activation towards a Th1 phenotype, and immune semaphorins. This regulation seems to be specific for the liver since visceral adipose tissue expression and serum levels of MCP1, IP10, TNFα and IL6 were not modified. Importantly, 47 other genes were already upregulated in histologically normal liver (e.g. CRP, Toll-like receptor (TLR) pathway). Interestingly, serum palmitate, known to activate the TLR pathway, was increased with steatosis. CONCLUSION/SIGNIFICANCE: The liver of obese patients without histological abnormalities already displayed a low-grade inflammation and could be more responsive to activators of the TLR pathway. NASH was then characterized by a specific gene signature. These findings help to identify new potential actors of the pathogenesis of 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.