Abstract

A high proportion of critically ill patients with coronavirus disease 2019 (COVID-19) experience thrombosis, and there is a strong correlation between anticoagulant therapy and the COVID-19 survival rate, indicating that common COVID-19 and thrombosis targets have potential therapeutic value for severe COVID-19.Gene expression profiling data were downloaded from Gene Expression Omnibus (GEO), and common differentially expressed genes (co-DEGs) were identified. The potential biological functions of these co-DEGs were explored by functional enrichment analysis, and protein–protein interaction (PPI) networks were constructed to elucidate the molecular mechanisms of the co-DEGs. Finally, hub genes in the co-DEG network were identified, and correlation analysis was performed.We identified 8320 upregulated genes and 7651 downregulated genes from blood samples of COVID-19 patients and 368 upregulated genes and 240 downregulated genes from blood samples of thrombosis patients. The enriched cellular component terms were mainly related to cytosolic ribosomes and ribosomal subunits. The enriched molecular function terms were mainly related to structural constituents of ribosomes and electron transfer activity. Construction of the PPI network and identification of hub genes ultimately confirmed that RPS7, IGF1R, DICER1, ERH, MCTS1, and TNPO1 were jointly upregulated hub genes, and FLNA and PXN were jointly downregulated hub genes.The identification of novel potential biomarkers provides new options for treating COVID-19-related thrombosis and reducing the rate of severe COVID-19.

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