ArticleArchives of medical science : AMS2020
Identification of key pathways and genes in nonalcoholic fatty liver disease using bioinformatics analysis.
Article in Archives of medical science : AMS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Integrated bioinformatics and SEM analysis reveal GPAM as a key mediator of fibrosis in NAFLD with metabolic dysfunction.Journal of genetics · 2026Article
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- Kaempferol Alleviates Hepatic Injury in Nonalcoholic Steatohepatitis (NASH) by Suppressing Neutrophil-Mediated NLRP3-ASC/TMS1-Caspase 3 Signaling.Molecules (Basel, Switzerland) · 2024Article
- Transcriptomic signatures of progressive and regressive liver fibrosis and portal hypertension.iScience · 2024Article
- Microarray-based Detection of Critical Overexpressed Genes in the Progression of Hepatic Fibrosis in Non-alcoholic Fatty Liver Disease: A Protein-protein Interaction Network Analysis.Current medicinal chemistry · 2024Article
- Genetic and epigenetic determinants of non-alcoholic fatty liver disease (NAFLD) in lean individuals: a systematic review.Translational gastroenterology and hepatology · 2024Review
- Proangiogenic role of circRNA-007371 in liver fibrosis.Cell proliferation · 2023Article
- Non-alcoholic fatty liver disease, metabolic syndrome, and type 2 diabetes mellitus: where do we stand today?Archives of medical science : AMS · 2023Article
- Mechanism of action ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022Article
- Network pharmacology analysis to explore mechanism of Three Flower Tea against nonalcoholic fatty liver disease with experimental support using high-fat diet-induced rats.Chinese herbal medicines · 2022Article
- Kaempferol Alleviates Steatosis and Inflammation During Early Non-Alcoholic Steatohepatitis Associated With Liver X Receptor α-Lysophosphatidylcholine Acyltransferase 3 Signaling Pathway.Frontiers in pharmacology · 2021Article
- Cellular Mechanisms of Liver Fibrosis.Frontiers in pharmacology · 2021Review
- Combined Analysis of Expression Profiles in a Mouse Model and Patients Identified BHMT2 as a New Regulator of Lipid Metabolism in Metabolic-Associated Fatty Liver Disease.Frontiers in cell and developmental biology · 2021Article
- Bioinformatics Analysis Explores Potential Hub Genes in Nonalcoholic Fatty Liver Disease.Frontiers in genetics · 2021Article
- Integrated Multichip Analysis Identifies Potential Key Genes in the Pathogenesis of Nonalcoholic Steatohepatitis.Frontiers in endocrinology · 2020Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionNonalcoholic fatty liver disease (NAFLD) is one of the most common types of liver disease in the world. However, the molecular mechanisms regulating the development of NAFLD have remained unclear. MATERIAL AND
methodsIn the present study, we analyzed two public datasets (GSE48452 and GSE89632) to identify differentially expressed mRNAs in the progression of NAFLD. Next, we performed bioinformatics analysis to explore key pathways underlying NAFLD development.
resultsGene Ontology (GO) analysis showed that differentially expressed genes (DEGs) were mainly involved in regulating a series of metabolism-related pathways (including proteolysis and lipid metabolism), cell proliferation and adhesion, the inflammatory response, and the immune response. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that DEGs in NAFLD were mainly enriched in the insulin signaling pathway, peroxisome proliferator-activated receptor (PPAR) signaling pathway, and p53 signaling pathway. We also constructed protein-protein interaction (PPI) networks for these DEGs. Interestingly, we observed that key hub nodes in PPI networks were also associated with the progression of hepatocellular carcinoma (HCC).
conclusionsTaken together, our analysis revealed that a series of pathways, such as metabolism and PPAR signaling pathways, were involved in NAFLD development. Moreover, we observed that many DEGs in NAFLD were also dysregulated in HCC. Although further validation is still needed, we believe this study could provide useful information to explore the potential candidate biomarkers for diagnosis, prognosis, and drug targets of NAFLD.
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