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The aim of this study was to identify potential markers of atherosclerosis development in familial hypercholesterolemia (FH) patients. GSE13985 microarray data, generated using blood samples from 5 FH patients and 5 matched controls, was downloaded from the Gene Expression Omnibus. Differentially expressed genes (DEGs) between FH and controls were identified and a protein-protein interaction (PPI) network was constructed. Module and hub proteins were screened in this network. The module genes were subjected to a gene ontology (GO) analysis, and a Kyoto Encyclopedia of Genes and Genomes enrichment analysis was also performed. A total of 394 genes, including 125 up- and 269 down-regulated genes, were differentially expressed. Ribosomal proteins L9 (RPL9), L35 (RPL35), and S7 (RPS7) were designated as hub nodes in the PPI network. The DEGs were found to be significantly enriched in ribosomal and oxidative phosphorylation pathways. Ribosomal protein genes were found to be involved in the ribosomal pathway. The cytochrome-c oxidase (COX) genes COX subunit VIIa polypeptide 2 (COX7A2), COX subunit VIIb (COX7B), COX subunit VIIc (COX7C), and COX subunit VIc (COX6C) were enriched in the oxidative phosphorylation pathway. Module analysis and GO enrichment analysis identified ribosomal proteins as important regulators of FH. Ribosomal and oxidative phosphorylation pathways may be closely associated with atherosclerosis development. Ribosomal protein genes and cytochrome-coxidase genes may be potential therapeutic targets for atherosclerosis.

Prediction of genetic risk factors of atherosclerosis using various bioinformatic tools