E-GEOD-49541
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-49541 | ExpressionAtlas | 2020-04-16
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-49541-analysis-methods.tsv | Tabular | |||
| E-GEOD-49541-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-49541-configuration.xml | Xml | |||
| E-GEOD-49541-percentile-ranks.tsv | Tabular | |||
| E-GEOD-49541.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 39 |
Similar Datasets
Project description:Expression data for Nonalcoholic fatty liver disease patients
| PRJNA214553 | ENA
Project description:Mardinoglu2014 - Genome-scale metabolic model
(HMR version 2.0) - human hepatocytes (iHepatocytes2322)
This model is described in the article:
Genome-scale metabolic
modelling of hepatocytes reveals serine deficiency in patients
with non-alcoholic fatty liver disease.
Mardinoglu A, Agren R, Kampf C,
Asplund A, Uhlen M, Nielsen J.
Nat Commun 2014; 5: 3083
Abstract:
Several liver disorders result from perturbations in the
metabolism of hepatocytes, and their underlying mechanisms can
be outlined through the use of genome-scale metabolic models
(GEMs). Here we reconstruct a consensus GEM for hepatocytes,
which we call iHepatocytes2322, that extends previous models by
including an extensive description of lipid metabolism. We
build iHepatocytes2322 using Human Metabolic Reaction 2.0
database and proteomics data in Human Protein Atlas, which
experimentally validates the incorporated reactions. The
reconstruction process enables improved annotation of the
proteomics data using the network centric view of
iHepatocytes2322. We then use iHepatocytes2322 to analyse
transcriptomics data obtained from patients with non-alcoholic
fatty liver disease. We show that blood concentrations of
chondroitin and heparan sulphates are suitable for diagnosing
non-alcoholic steatohepatitis and for the staging of
non-alcoholic fatty liver disease. Furthermore, we observe
serine deficiency in patients with NASH and identify PSPH,
SHMT1 and BCAT1 as potential therapeutic targets for the
treatment of non-alcoholic steatohepatitis.
This model is hosted on
BioModels Database
and identified by:
MODEL1402200003.
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To the extent possible under law, all copyright and related or
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2005-01-01 | MODEL1402200003 | BioModels
Project description:To investigate the function of miRNAs in liver, we obtained liver tissues from nonsteatotic individuals and fatty livers from patients with nonalcoholic fatty liver disease (NAFLD). Patients due to excessive alcohol consumption, autoimmune liver disease, viral hepatitis and diabetes were excluded. Nonsteatotic livers were collected from the normal region of the livers from donors who received liver resection due to liver hemangioma, and were defined as those with NASH activity scores of 0 We then performed miRNA sequencing using livers from two NAFLD patients and two nonsteatotic individuals.
2023-03-12 | GSE227021 | GEO
Project description:Expression data from human non-alcoholic fatty liver disease stages
| PRJNA266543 | ENA
Project description:Non-alcoholic fatty liver disease (NAFLD) is a predominant form of chronic liver disease, affecting nearly 25 % of the global population. The progression from steatosis to nonalcoholic steatohepatitis (NASH) in NAFLD patients is one of the major causes of liver-related death worldwide. We assessed the miRNA expression profiles of the exosomes derived from the peripheral blood of NASH patients or healthy controls.
2022-06-01 | GSE202167 | GEO
Project description:Expression data from human non-alcoholic fatty liver disease stages
2020-11-27 | E-GEOD-63067 | ExpressionAtlas
Project description:Expression data from kidney biopsies of liver disease patients
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Project description:Chronic liver diseases are worldwide on the rise. Due to the rapidly increasing incidence, in particular in Western countries, non-alcoholic fatty liver disease (NAFLD) is gaining importance. As the disease progresses it can develop into hepatocellular carcinoma. Lipid accumulation in hepatocytes has been identified as the characteristic structural change in NAFLD development, but the molecular mechanisms responsible for disease development remained unresolved. Here, we uncover a strong downregulation of the PI3K-AKT pathway and an upregulation of the MAPK pathway in primary hepatocytes from a preclinical model fed with a Western diet (WD). Dynamic pathway modeling of hepatocyte growth factor (HGF) signal transduction combined with global proteomics identifies that an elevated basal MET phosphorylation rate is the main driver of altered signaling leading to increased proliferation of WD-hepatocytes. Model-adaptation to patient-derived hepatocytes reveals a patient-specific variability in basal MET phosphorylation, which correlates with the outcome of patients after liver surgery. Thus, dysregulated basal MET phosphorylation could be an indicator for the health status of the liver and thereby inform on the risk of a patient to suffer from liver failure after surgery.
2024-01-16 | MODEL2306280002 | BioModels
Project description:Background and aim: The Insulin-like growth factor (IGF) axis is increasingly suggested to be involved in fatty liver disease and progression. We identified IGFBP2 as transcriptional regulatory effect network in liver steatosis and conducted a translational approach of its role in liver pathology from mouse to human, and whether it is influenced by conventional clinical intervention that mitigate hepatic steatosis. Methods: Primary hepatocytes from either C57Bl6 controls, alb-SREBP-1c mice with moderate transgene induced hepatic lipid accumulation or aP2-SREBP-1c mice with massive ectopic hepatic lipid accumulation, were analyzed to identify regulatory networks based on differentially regulated hepatic gene expression. In a translational approach, serum of morbidly obese patients with and without diabetes and biopsy-proven NAFLD were used for ELISA-based validation of mouse data. Moreover, sera of patients undergoing intervention were analyzed and correlated to liver fat content. Results: Comparative knowledge-based transcriptome analysis identified IGFBP2 as top score regulatory effect network between moderate and aggravated fatty liver in mouse models. The reduced expression of IGFBP2 in aP2-SREPB-1c progressed fatty liver associated with Igfbp2 promoter hypermethylation. Reduced secretion of IGFBP2 from aP2-SREBP-1c hepatocytes was reflected in the circulation of the animals. In this phenotype, reductions of IGFBP2 were accompanied by reduced fatty acid oxidation and increased methyltransferase and SIRT activity. Physiologically, IGFBP2 has no direct impact on lipid metabolism but might modulate IGF1 action on de novo lipogenesis. In humans, IGFBP2 levels declined from non-obese men to morbidly obese men with NAFLD and NASH. In intervention study reductions in liver fat correlated with restoration of IGFBP2 serum levels to values found in healthy individuals in morbidly obese patients following bariatric surgery. Conclusion: In hepatic metabolism changes of IGFBP2 abundance is connected to lipid metabolism whereas changes in IGFBP2 secretion were directly reflected in the circulation. IGFBP2 serum concentration correlates with the degree of fatty liver, which seems to be related to plasticity of the adipose tissue. These data provide IGFBP2 as a potential non-invasive biomarker for fatty liver disease directly reflecting the degree of impaired liver function with the potential to indicate progressed fatty liver disease.
2020-06-29 | GSE139901 | GEO