tetano
Editor, Senior Moderator
PLoS One
. 2022 Jan 19;17(1):e0262737.
doi: 10.1371/journal.pone.0262737. eCollection 2022.
Identification of hub genes associated with COVID-19 and idiopathic pulmonary fibrosis by integrated bioinformatics analysis
Qianyi Chen[SUP] 1 [/SUP], Shilin Xia[SUP] 2 3 [/SUP], Hua Sui[SUP] 1 [/SUP], Xueying Shi[SUP] 1 2 [/SUP], Bingqian Huang[SUP] 1 2 [/SUP], Tingxin Wang[SUP] 1 [/SUP]
Affiliations
Abstract
Introduction: The coronavirus disease 2019 (COVID-19), emerged in late 2019, was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The risk factors for idiopathic pulmonary fibrosis (IPF) and COVID-19 are reported to be common. This study aimed to determine the potential role of differentially expressed genes (DEGs) common in IPF and COVID-19.
Materials and methods: Based on GEO database, we obtained DEGs from one SARS-CoV-2 dataset and five IPF datasets. A series of enrichment analysis were performed to identify the function of upregulated and downregulated DEGs, respectively. Two plugins in Cytoscape, Cytohubba and MCODE, were utilized to identify hub genes after a protein-protein interaction (PPI) network. Finally, candidate drugs were predicted to target the upregulated DEGs.
Results: A total of 188 DEGs were found between COVID-19 and IPF, out of which 117 were upregulated and 71 were downregulated. The upregulated DEGs were involved in cytokine function, while downregulated DEGs were associated with extracellular matrix disassembly. Twenty-two hub genes were upregulated in COVID-19 and IPF, for which 155 candidate drugs were predicted (adj.P.value < 0.01).
Conclusion: Identifying the hub genes aberrantly regulated in both COVID-19 and IPF may enable development of molecules, encoded by those genes, as therapeutic targets for preventing IPF progression and SARS-CoV-2 infections.
. 2022 Jan 19;17(1):e0262737.
doi: 10.1371/journal.pone.0262737. eCollection 2022.
Identification of hub genes associated with COVID-19 and idiopathic pulmonary fibrosis by integrated bioinformatics analysis
Qianyi Chen[SUP] 1 [/SUP], Shilin Xia[SUP] 2 3 [/SUP], Hua Sui[SUP] 1 [/SUP], Xueying Shi[SUP] 1 2 [/SUP], Bingqian Huang[SUP] 1 2 [/SUP], Tingxin Wang[SUP] 1 [/SUP]
Affiliations
- PMID: 35045126
- DOI: 10.1371/journal.pone.0262737
Abstract
Introduction: The coronavirus disease 2019 (COVID-19), emerged in late 2019, was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The risk factors for idiopathic pulmonary fibrosis (IPF) and COVID-19 are reported to be common. This study aimed to determine the potential role of differentially expressed genes (DEGs) common in IPF and COVID-19.
Materials and methods: Based on GEO database, we obtained DEGs from one SARS-CoV-2 dataset and five IPF datasets. A series of enrichment analysis were performed to identify the function of upregulated and downregulated DEGs, respectively. Two plugins in Cytoscape, Cytohubba and MCODE, were utilized to identify hub genes after a protein-protein interaction (PPI) network. Finally, candidate drugs were predicted to target the upregulated DEGs.
Results: A total of 188 DEGs were found between COVID-19 and IPF, out of which 117 were upregulated and 71 were downregulated. The upregulated DEGs were involved in cytokine function, while downregulated DEGs were associated with extracellular matrix disassembly. Twenty-two hub genes were upregulated in COVID-19 and IPF, for which 155 candidate drugs were predicted (adj.P.value < 0.01).
Conclusion: Identifying the hub genes aberrantly regulated in both COVID-19 and IPF may enable development of molecules, encoded by those genes, as therapeutic targets for preventing IPF progression and SARS-CoV-2 infections.