ArticleHepatitis monthly2015
Molecular mechanisms for alcoholic hepatitis based on analysis of gene expression profile.
Article in Hepatitis monthly, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed, 14 citations in OpenAlex.
- Proteomic analysis of alcohol-associated hepatitis reveals glycoprotein NMB (GPNMB) as a novel hepatic and serum biomarker.Alcohol (Fayetteville, N.Y.) · 2022Article
- Association between the expression of carbonic anhydrase II and clinicopathological features of hepatocellular carcinoma.Oncology letters · 2019Article
- TSPO PET Imaging: From Microglial Activation to Peripheral Sterile Inflammatory Diseases?Contrast media & molecular imaging · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlcoholic hepatitis (AH) is an acute manifestation of alcoholic liver disease with high mortality rates.
objectivesOur aim was to study the molecular mechanisms of AH. MATERIALS AND
methodsThe differentially expressed genes (DEGs) in liver between AH and control cases were identified by analyzing the GSE28619 microarray data using t-test. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and Gene Ontology (GO) enrichment analyses were performed using DAVID online tool. The protein-protein interaction (PPI) network was constructed using Search Tool for the Retrieval of Interacting Genes (STRING) and the subnetwork was identified by BioNet. Both PPI network and subnetwork were visualized using the Cytoscape software.
resultsTotal 908 DEGs (551 up- and 357 down-regulated DEGs) were obtained. The up-regulated DEGs were significantly enriched in 15 pathways and 112 GO biological processes. The down-regulated DEGs were significantly enriched in 22 pathways and 84 GO biological processes. The PPI network with 608 nodes and 2878 interactions was constructed and the subnetwork with 53 nodes and 131 interactions was also identified. The hub DEGs (TSPO, PPIB, NME1 and NME2) were extracted in this subnetwork.
conclusionsTSPO might contribute to the liver damage and AH progression induced by mitochondrial dysfunction through oxidative stress of liver. TSPO interacted with PPIB might play important roles in liver damage in AH. The interaction between NME1 and NME2 might contribute to the transformation from AH to hepatocellular carcinoma.
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