ArticleJCI insight2017
Interspecies NASH disease activity whole-genome profiling identifies a fibrogenic role of PPARα-regulated dermatopontin.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 2 of them syntheses that pooled it.
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.
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Who cites it
84 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.
- Comprehensive meta-analysis reveals distinct gene expression signatures of MASLD progression.Life science alliance · 2024Pooled it
- Hepatic steatosis and steatohepatitis: a functional meta-analysis of sex-based differences in transcriptomic studies.Biology of sex differences · 2021Pooled it
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Intestinal FXR deficiency uncouples steatosis protection from liver inflammation and fibrosis in MASH-diet fed mice.Scientific reports · 2026Article
- Article
- Sleeve Gastrectomy Alters Exosomal miR-497-5p Cargo to Ameliorate Metabolic Dysfunction-Associated Steatotic Liver by Targeting GABARAPL1.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Plasticity of Epigenomic and Transcriptomic Aging Reveals Common Targets for Reprogramming by Environmental Exposures.Research square · 2025Article
- Gradual DNA methylation changes reveal transcription factors implicated in metabolic dysfunction-associated steatotic liver disease progression and epigenetic age acceleration.Clinical epigenetics · 2025Article
- Review
- Targeting senescent hepatocytes for treatment of metabolic dysfunction-associated steatotic liver disease and multi-organ dysfunction.Nature communications · 2025Article
- Unraveling Metabolic Dysfunction-Associated Steatotic Liver Disease Through the Use of Omics Technologies.International journal of molecular sciences · 2025Review
- Tumor-associated neutrophils attenuate the immunosensitivity of hepatocellular carcinoma.The Journal of experimental medicine · 2025Article
- Data-driven cluster analysis identifies distinct types of metabolic dysfunction-associated steatotic liver disease.Nature medicine · 2024Article
- Inhibition of hepatic oxalate overproduction ameliorates metabolic dysfunction-associated steatohepatitis.Nature metabolism · 2024Article
- Identification of HTRA1, DPT and MXRA5 as potential biomarkers associated with osteoarthritis progression and immune infiltration.BMC musculoskeletal disorders · 2024Article
- High-Protein Mulberry Leaves Improve Glucose and Lipid Metabolism via Activation of the PI3K/Akt/PPARα/CPT-1 Pathway.International journal of molecular sciences · 2024Article
- Article
- Emerging Insights into the Role of BDNF on Health and Disease in Periphery.Biomolecules · 2024Review
- Digital pathology with artificial intelligence analysis provides insight to the efficacy of anti-fibrotic compounds in human 3D MASH model.Scientific reports · 2024Article
- Integrated analysis of differentially expressed genes and miRNA expression profiles in dilated cardiomyopathy.Heliyon · 2024Article
24 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
24 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease prevalence is soaring with the obesity pandemic, but the pathogenic mechanisms leading to the progression toward active nonalcoholic steatohepatitis (NASH) and fibrosis, major causes of liver-related death, are poorly defined. To identify key components during the progression toward NASH and fibrosis, we investigated the liver transcriptome in a human cohort of NASH patients. The transition from histologically proven fatty liver to NASH and fibrosis was characterized by gene expression patterns that successively reflected altered functions in metabolism, inflammation, and epithelial-mesenchymal transition. A meta-analysis combining our and public human transcriptomic datasets with murine models of NASH and fibrosis defined a molecular signature characterizing NASH and fibrosis and evidencing abnormal inflammation and extracellular matrix (ECM) homeostasis. Dermatopontin expression was found increased in fibrosis, and reversal of fibrosis after gastric bypass correlated with decreased dermatopontin expression. Functional studies in mice identified an active role for dermatopontin in collagen deposition and fibrosis. PPARα activation lowered dermatopontin expression through a transrepressive mechanism affecting the Klf6/TGFβ1 pathway. Liver fibrotic histological damages are thus characterized by the deregulated expression of a restricted set of inflammation- and ECM-related genes. Among them, dermatopontin may be a valuable target to reverse the hepatic fibrotic process.
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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.