Network-based transcriptomic analysis identifies the genetic effect of COVID-19 to chronic kidney disease patients: A bioinformatics approach

10, June 2021 |

Authors:

Abstract

COVID-19 has emerged as global health threats. Chronic kidney disease (CKD) patients are immune- compromised and may have a high risk of infection by the SARS-CoV-2. We aimed to detect common transcriptomic signatures and pathways between COVID-19 and CKD by systems biology analysis. We analyzed transcriptomic data obtained from peripheral blood mononuclear cells (PBMC) infected with SARS-CoV-2 and PBMC of CKD patients. We identified 49 differentially expressed genes (DEGs) which were common between COVID-19 and CKD. The gene ontology and pathways analysis showed the DEGs were associated with ‘‘platelet degranulation”, ‘‘regulation of wound healing”, ‘‘platelet activation”, ‘‘focal adhesion”, ‘‘regulation of actin cytoskeleton” and ‘‘PI3K-Akt signalling pathway”. The protein- protein interaction (PPI) network encoded by the common DEGs showed ten hub proteins (EPHB2, PRKAR2B, CAV1, ARHGEF12, HSP90B1, ITGA2B, BCL2L1, E2F1, TUBB1, and C3). Besides, we identified sig- nificant transcription factors and microRNAs that may regulate the common DEGs. We investigated protein-drug interaction analysis and identified potential drugs namely, aspirin, estradiol, rapamycin, and nebivolol. The identified common gene signature and pathways between COVID-19 and CKD may be therapeutic targets in COVID-19 patients with CKD comorbidity.