Bioinformatics analysis of potential common pathogenic mechanisms for COVID-19 and venous thromboembolism

Background: A growing body of research has shown that patients with coronavirus disease 2019 (COVID-19) have significantly higher rates of venous thromboembolism (VTE) than healthy. However, the mechanism remains incompletely elucidated. This study aimed to further investigate the molecular mechanisms underlying the development of this complication. Methods: The gene expression profiles of COVID-19 and VTE were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the common differentially expressed genes (DEGs) for COVID-19 and VTE, functional annotation, a protein-protein interactions (PPI) network, module construction, and hub gene identification were performed. Finally, we constructed a transcription factor (TF)-gene regulatory network and a TF-miRNA regulatory network for hub genes. Results: A total of 42 common DEGs were selected for subsequent analyses. Functional analyses showed that biological function and signaling pathways collectively participated in the development and progression of VTE and COVID-19. Finally, 8 significant hub genes were identified using the cytoHubba plugin, including RSL24D1, RPS17, RPS27, HINT1, COX7C, RPL35, RPL34, and NDUFA4, which had preferable values as diagnostic markers for COVID-19 and VTE. Conclusions: Our study revealed the common pathogenesis of COVID-19 and VTE. These common pathways and pivotal genes may provide new ideas for further mechanistic studies.