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10.7717/peerj.10336

http://scihub22266oqcxt.onion/10.7717/peerj.10336
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33240650!7678445!33240650
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suck abstract from ncbi

pmid33240650      PeerJ 2020 ; 8 (?): e10336
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  • Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development #MMPMID33240650
  • Zhang K; Qin X; Zhou X; Zhou J; Wen P; Chen S; Wu M; Wu Y; Zhuang J
  • PeerJ 2020[]; 8 (?): e10336 PMID33240650show ga
  • BACKGROUND: Foam cells (FCs) play crucial roles in the process of all stages of atherosclerosis. Smooth muscle cells (SMCs) and macrophages are the major sources of FCs. This study aimed to identify the common molecular mechanism in these two types of FCs. METHODS: GSE28829, GSE43292, GSE68021, and GSE54666 were included to identify the differentially expressed genes (DEGs) associated with FCs derived from SMCs and macrophages. Gene Ontology biological process (GO-BP) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed by using the DAVID database. The co-regulated genes associated with the two origins of FCs were validated (GSE9874), and their expression in vulnerable atherosclerosis plaques (GSE120521 and GSE41571) was assessed. RESULTS: A total of 432 genes associated with FCs derived from SMCs (SMC-FCs) and 81 genes associated with FCs derived from macrophages (M-FCs) were identified, and they were mainly involved in lipid metabolism, inflammation, cell cycle/apoptosis. Furthermore, three co-regulated genes associated with FCs were identified: GLRX, RNF13, and ABCA1. These three common genes showed an increased tendency in unstable or ruptured plaques, although in some cases, no statistically significant difference was found. CONCLUSIONS: DEGs related to FCs derived from SMCs and macrophages have contributed to the understanding of the molecular mechanism underlying the formation of FCs and atherosclerosis. GLRX, RNF13, and ABCA1 might be potential targets for atherosclerosis treatment.
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