Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1194226 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31611630_1.fastq.gz | Fastqsanger.gz | |||
| SRR31611630_2.fastq.gz | Fastqsanger.gz | |||
| SRR31611631_1.fastq.gz | Fastqsanger.gz | |||
| SRR31611631_2.fastq.gz | Fastqsanger.gz | |||
| SRR31611632_1.fastq.gz | Fastqsanger.gz |
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Project description:Liver cirrhosis is one of the leading causes of decreased life expectancy worldwide. However, the molecular mechanisms underlying the development of liver cirrhosis remain unclear. In this study, we performed a comprehensive analysis using transcriptome sequencing to explore the genes, pathways, and interactions associated with liver cirrhosis. We performed transcriptome sequencing of blood samples from patients with cirrhosis and healthy controls (1:1 matched for sex and age). For transcriptome analysis, we screened for differentially expressed miRNAs and mRNAs, analyzed mRNAs to identify possible core genes and pathways, and performed co-analysis of miRNA and mRNA sequencing results. And we validated differentially expressed microRNA (miRNA) and mRNAs using real-time quantitative polymerase chain reaction. Using a systems biology framework, We identified miRNAs and mRNAs that were differentially expressed in the blood of cirrhotic patients and healthy controls. And explored associated pathways as well as disease-specific networks.
2025-08-01 | GSE210545 | GEO
Project description:Male rats received repeated low-dose diethylnitrosamine (DEN) to induce liver cirrhosis, and were treated with nizatidine to examine change of liver transcriptome and its association with liver cancer chemopreventive effect of nizatidine.
2021-06-28 | GSE115473 | GEO
Project description:Background and aims: Extrahepatic organ failures are key determinants of acute-on-chronic liver (ACLF), and thereby of short-term mortality of liver cirrhosis. While the role of systemic inflammation and mitochondrial dysfunction in the pathogenesis of ACLF is well known, the contribution of the liver itself is less understood. In the present study, we therefore investigated signatures in the hepatic transcriptome in ACLF versus compensated and decompensated liver cirrhosis. Methods: Bulk-RNA sequencing and spatial transcriptomics were performed in liver specimens from patients with compensated cirrhosis, decompensated cirrhosis or ACLF undergoing liver transplantation. In addition, a detailed analysis of genes involved in energy metabolism and associated substrates was performed. Results: ACLF was associated with changes in the hepatic transcriptome, clearly distinct from compensated and decompensated cirrhosis. Most strongly downregulated in ACLF were pathways involved in substrate metabolism and mitochondrial function, and – more specifically - ACLF was characterized by downregulation of multiple genes involved in glucose and amino acid metabolism. In line, spatial transcriptomics data revealed a breakdown of the functional liver zonation in ACLF, with decreasing proportions of hepatocytes specialized in gluconeogenesis/beta-oxidation. BCKDK, which was strongly downregulated in ACLF, was identified as a potential candidate gene linking impaired metabolism of branched-chain amino acids with impaired glucose metabolism. Conclusion: ACLF is characterized by distinct changes in the hepatic transcriptome, which affect key pathways in substrate metabolism and mitochondrial function and are associated with a loss of the functional liver zonation. Downregulation of BCKDK in ACLF might be of particular interest, as it may integrate metabolism of branched-chained amino acids with impaired glucose metabolism and mitochondrial dysfunction.
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Project description:Transcriptome analysis of liver cirrhosis
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Project description:The aim of this study is to compare post-hepatitis C virus (HCV) and post-alcoholism cirrhosis gene expression profiling. By transcriptome analysis with a cDNA array virtually covering every transcript in liver, we compared transcript levels in alcoholic- , HCV-cirrhosis and control liver. A stringent selection identified a list of 70 transcripts which completely separated the 3 groups of patients (7 HCV-cirrhosis, 7 alcoholic cirrhosis and 8 control livers). In contrast, in an hepatocellular carcinoma (HCC) context, comparison of 10 HCV-cirrhosis, 10 alcoholic cirrhosis and the 8 control livers failed to identify such transcripts. We report that dysregulations at the transcriptional level do exist in HCC-free cirrhosis, are transiently observed prior to detectable HCC. Keywords: etiology-dependent and HCC-dependent analysis
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2011-11-02 | E-GEOD-22977 | biostudies-arrayexpress
Project description:Gene-expression profiles of hepatitis C-related, early-stage liver cirrhosis Background & Aims: Liver cirrhosis affects 1%M-bM-^HM-^R2% of population and is the major risk factor of hepatocellular carcinoma (HCC). Hepatitis C cirrhosis-related HCC is the most rapidly increasing cause of cancer death in the US. Non-invasive methods have been developed to identify patients with asymptomatic, early-stage cirrhosis, increasing the burden of HCC surveillance, but biomarkers are needed to identify patients with cirrhosis who are most in need of surveillance. We investigated whether a liver-derived 186-gene signature previously associated with outcomes of patients with HCC is prognostic for patients newly diagnosed with cirrhosis but without HCC. Methods: We performed gene expression profile analysis of formalin-fixed needle biopsies from the livers of 216 patients with hepatitis C-related early-stage (Child-Pugh class A) cirrhosis who were prospectively followed for a median of 10 years at an Italian center. We evaluated whether the 186-gene signature was associated with death, progression of cirrhosis, and development of HCC. Results: Fifty-five (25%), 101 (47%), and 60 (28%) patients were classified as having poor-, intermediate-, and good-prognosis signatures, respectively. In multivariable Cox regression modeling, the poor-prognosis signature was significantly associated with death (P=.004), progression to advanced cirrhosis (P<.001), and development of HCC (P=.009). The 10-year rates of survival were 63%, 74%, and 85% and the annual incidences of HCC were 5.8%, 2.2%, and 1.5% for patients with poor-, intermediate-, and good-prognosis signatures, respectively. Conclusions: A 186-gene signature used to predict outcomes of patients with HCC is also associated with outcomes of patients with hepatitis C-related early-stage cirrhosis. This signature might be used to identify patients with cirrhosis in most need of surveillance and strategies to prevent their development of HCC. 216 liver biopsy specimens
2013-01-22 | E-GEOD-15654 | biostudies-arrayexpress