Key result
Integrative bioinformatics analysis identified 9 energy metabolism-related hub genes, including CD36 and PRKAR2A which demonstrated high diagnostic accuracy (AUC=1.000), as potential biomarkers for pediatric NAFLD.
Why the study?
Pediatric NAFLD is associated with energy metabolism and risks hepatocellular carcinoma if unaddressed, motivating study into its underlying mechanisms, potential biomarkers, and therapeutic targets.
Observational (n=57)
Bioinformatics analysis identified 9 energy metabolism-related hub genes that may serve as diagnostic biomarkers or therapeutic targets for pediatric non-alcoholic fatty liver disease.
Potential energy metabolism genes emerge as pediatric NAFLD biomarkers; leaves open clinical targets pending validation.
BACKGROUND: Pediatric non-alcoholic fatty liver disease (NAFLD) is a chronic steatosis of the liver associated with energy metabolism in children and adolescents, failure to intervene promptly can elevate the risk of developing hepatocellular carcinoma. Therefore, this study aimed to understand the underlying mechanism of pediatric NAFLD and investigate potential biomarkers and therapeutic targets. METHODS: We investigated genes using the GSE185051 data set related to energy metabolism from the GeneCards database, constructed protein-protein interaction network, identified hub genes and established networks representing interactions between these hub genes and miRNA, RNA-binding proteins, transcription factors, and drugs. Subsequently, we performed Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis, Gene Set Enrichment Analysis (GSEA), and immune infiltration analysis. RESULTS: Our analysis identified 9 hub genes through the PPI network. The target molecules were identified through the interaction network between hub genes and miRNAs, RNA-binding proteins, transcription factors, and drugs. GO analysis revealed that hub genes were associated with oxidative stress responses and other pathways. KEGG analysis highlighted their involvement in pathways such as insulin resistance, among others. GSEA revealed that hub genes were highly enriched in pathways related to Omega-9 fatty acid synthesis, among others. Immune infiltration analysis suggested that mast cells and T follicular helper cells play significant roles in the pathogenesis of NAFLD. CONCLUSION: We identified the hub genes in pediatric NAFLD closely related to energy metabolism. These findings offer the potential for identifying potential novel diagnostic biomarkers, and establishing therapeutic targets for pediatric NAFLD.
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Yijun et al. (2024) conducted an observational in Pediatric non-alcoholic fatty liver disease (NAFLD) (n=57). Pediatric NAFLD vs. Healthy liver controls was evaluated on Identification of energy metabolism-related differentially expressed hub genes and their diagnostic accuracy (AUC). Integrative bioinformatics analysis identified 9 energy metabolism-related hub genes, including CD36 and PRKAR2A which demonstrated high diagnostic accuracy (AUC=1.000), as potential biomarkers for pediatric NAFLD.
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