Similar Datasets
Project description:Non-alcoholic fatty liver disease (NAFLD) is estimated to affect 25% of the world’s population and its prevalence is increasing with the rise in obesity. The evolution of this disease includes different pathological stages: steatosis, inflammation, fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Liver biopsy stands as the gold standard for NAFLD assessment despite its invasive nature and limited performance. Liver fibrosis is the most important clinical parameter, as it is closely related to mortality, and biopsies are only considered when advanced fibrosis is suspected. This scenario makes the finding of a non-invasive and reliable biomarker an urgent need for an accurate diagnosis. To this end, we first performed a discovery study on 159 plasma samples from histologically characterised NAFLD patients using mass spectrometry (MS)-based quantitative proteomics. Insulin-like growth factor-binding protein complex acid labile (ALS, P35858) and Galectin-3-binding protein (LG3BP, Q08380) were selected for a verification by enzyme-linked immunosorbent assay (ELISA) in the same cohort and finally validated in an independent NAFLD cohort of 200 plasma samples.ALS and LG3BP were validated as advanced liver fibrosis biomarkers and successfully included in a panel with FibroTest variables. ELISA kits availability would allow to achieve relatively fast clinical translation if further investigations in larger cohorts confirm these results.
2024-05-22 | PXD043340 | Pride
Project description:Non-alcoholic fatty liver disease (NAFLD), alongside the global obesity epidemic, is rapidly emerging as a dominant liver disease etiology that leads to progressive liver fibrosis, its terminal stage, cirrhosis, and hepatocellular carcinoma (HCC). We identified and validated a 133-gene signature (Prognostic Liver Signature for NAFLD [PLS-NAFLD]) to predict long-term HCC risk in patients with NAFLD. By analyzing PLS-NAFLD, IDO1 was identified as a potenial chemopreventive target for HCC from NAFLD. To test this hypothesis, we utilized our clinical-prognostic-signature-inducible cell culture model. We first confirmed that free fatty acid treatment (800 μM oleic acid and 400 μM palmitic acid) can induce PLS-NAFLD, then IDO1 inhibitor, epacadostat, can reverse the high-risk pattern in a dose-dependent manner.
2022-07-01 | GSE200460 | GEO
Project description:FLORINASH - The role of intestinal microflora in non-alcoholic fatty liver disease (NAFLD) EU FP7-HEALTH, project number 241913<br>Florinash examined the role on the gut microbiota in NAFLD. Metagenomic, proteomic, metabolomic and transcriptomic data were integrated to give provide a systems biology approach to disease-associated studies. Liver biopsies were obtained from patients undergoing bariatric surgery; one was used to diagnose NAFLD, the other was used to examine the host transcriptome in NAFLD. This dataset is part of the TransQST collection.
2018-03-15 | E-MTAB-4856 | biostudies-arrayexpress
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:Melatonin has been reported to improve NAFLD, exploring the underlying mechanisms will be beneficial for better treatment of NAFLD. CDHFD- and MCD-fed mice with melatonin intervention exhibited significantly decreased liver steatosis, lobular inflammation, and focal liver necrosis. Single-cell RNA sequencing revealed melatonin selectively inhibited proinflammatory CCR3+ MoMFs, and upregulated anti-inflammatory CD206+ MoMFs in NAFLD mice. Hepatic infiltrated CCR3+CD14+ MoMFs is also significantly increased in patients with NAFLD. Mechanistically, melatonin receptor independent BTG2-ATF4 signaling plays a vital role in the regulation of CCR3+ MoMFs endoplasmic reticulum stress, survival, and proinflammation by melatonin. In contrast, melatonin upregulated CD206+ MoMFs survival and polarization via MT1/2 receptors. Melatonin stimulation also regulates human CCR3+ MoMFs and CD206+ MoMFs survival and inflammation in vitro. Furthermore, CCR3 depletion antibody monotherapy decreased liver inflammation and improved NAFLD in mice. Thus, Therapies targeting CCR3+ MoMFs may have potential benefits in NAFLD treatment.
2023-06-04 | GSE204821 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) is a common liver disorder and affects approximately one third of the general population.Recent studies have shown that long non-coding (lncRNA) plays critical roles in a myriad of biological processes and human diseases,Since the roles of lncRNA in NAFLD remain unknown,they were investigated in the study.Our findings indicate that the expression profiles of lncRNAs has changed in NAFLD as compared with normal liver, and may provide novel insight into the molecular mechanism underlying the disease and potential novel diagnostic or therapeutic targets for NAFLD. Microarray expression profiling of mRNAs and lncRNAs were conducted using RNA extracted from five NAFLD liver tissues and five normal liver samples.
2015-09-08 | E-GEOD-72756 | biostudies-arrayexpress
Project description:determine the effect of the high-fat diet on the proteomics profile of liver tissue.Mice were fed with HFD for 16 weeks to establish a NAFLD mouse model. Mice fed with normal chow diet were taken as controls. Five replicate liver samples were collected from each group for proteomics analysis.
2022-06-09 | PXD030727 | Pride
Project description:Background & Aims: Cirrhosis and liver cancer are potential outcomes of advanced nonalcoholic fatty liver disease (NAFLD). It is not clear what factors determine whether patients will develop advanced or mild NAFLD, limiting non-invasive diagnosis and treatment before clinical sequelae emerge. We investigated whether DNA methylation profiles can distinguish patients with mild disease from those with advanced NAFLD, and how these patterns are functionally related to hepatic gene expression. Methods: We collected frozen liver biopsies and clinical data from patients with biopsy-proven NAFLD (56 in the discovery cohort and 34 in the replication cohort). Samples were divided into groups based on histologic severity of fibrosis: F0?1 (mild) and F3?4 (advanced). DNA methylation profiles were determined and coupled with gene expression data from the same biopsies; differential methylation was validated in subsets of the discovery and replication cohorts. We then analyzed interactions between the methylome and transcriptome. Results: Clinical features did not differ between patients known to have mild or advanced fibrosis based on biopsy analysis. There were 69,247 differentially methylated CpG sites (76% hypomethylated, 24% hypermethylated) in patients with advanced vs mild NAFLD (P<.05). Methylation at FGFR2, MAT1A, and CASP1 was validated by bisulfite pyrosequencing and the findings were reproduced in the replication cohort. Methylation correlated with gene transcript levels for 7% of differentially methylated CpG sites, indicating that differential methylation contributes to differences in expression. In samples with advanced NAFLD, many tissue repair genes were hypomethylated and overexpressed, whereas genes in certain metabolic pathways, including 1-carbon metabolism, were hypermethylated and under-expressed. Conclusions: Functionally relevant differences in methylation can distinguish patients with advanced vs mild NAFLD. Altered methylation of genes that regulate processes such as steatohepatitis, fibrosis, and carcinogenesis indicate the role of DNA methylation in progression of NAFLD. Three technical replicates were included for quality control along with 35 mild NAFLD (33 unique samples) and 24 advanced NAFLD (23 unique sample). One sample per technical duplication was randomly included for a total of 56 NAFLD samples used for study.
2013-08-30 | E-GEOD-49542 | biostudies-arrayexpress
Project description:Emerging evidence suggests that microRNAs (miRNAs) are crucially involved in pathogenesis of NAFLD. The integrated analysis of expression profiles of miRNAs and mRNAs can be used to identify functional miRNA-target relationships with high precision. The purpose of this study was to provide insights into the immunopathogenesis of NAFLD using this integrated analysis method.Differentially expressed miRNAs and mRNAs of CD4+ T lymphocytes from liver and mesenteric lymph nodes(MLN) of NAFLD and normal mice were analyzed by microarrays and RNA sequencing respectively. Subsequently, the target genes of the differentially expressed miRNAs were predicted and overlapped with the differentially expressed mRNAs. Then, GO and pathway analyses were performed for the intersecting key genes. The microarray analysis indicated that 170 miRNAs and 2,791 mRNAs were significantly dysregulated in CD4+ T lymphocytes from liver between the two groups. Among the 2,791 mRNAs, 911 overlapped with putative miRNA target genes. A pathway analysis showed that the MAPK pathway was consistently enriched in the liver of NAFLD mice. miR-149-3p, miR-663a, miR-1908, miR-2861 and miR-3185 likely play important roles in the regulation of MAPK pathways. Furthermore, the Notch signaling pathway This study provides an integrated dataset of the miRNA and mRNA profiles in NAFLD, and the results demonstrate that not only the MAPK pathway and its related miRNAs but also the Notch pathway may be involved in NAFLD immunological development.
2014-10-23 | GSE62577 | GEO
Project description:Nonalcoholic fatty liver disease represents a spectrum of pathology that ranges from benign steatosis to potentially-progressive steatohepatitis and affects more than 30% of US adults. Advanced NAFLD is associated with increased morbidity and mortality from cirrhosis, primary liver cancer, cardiovascular disease and extrahepatic cancers. Accurate identification of patients at risk for advanced NAFLD is challenging. The aims of this study were to define the liver gene expression patterns that distinguish mild from advanced NAFLD and to develop a gene expression profile associated with advanced NAFLD. We analyzed total RNA from 72 patients with NAFLD (40 with mild NAFLD, fibrosis stage 0-1 and 32 with advanced NAFLD, fibrosis stage 3-4) and developed a gene profile associated with advanced NAFLD. This dataset is part of the TransQST collection.
2013-08-30 | E-GEOD-49541 | biostudies-arrayexpress