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CXCL10 May Be Responsible for Susceptibility to Pulmonary Embolism in COVID-19 Patients
Yingli Liu1, Dan Si2, Pingping Bai3
1Department of Pulmonary and Critical Care Medicine, Zhengzhou University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, Henan, 450003, People's Republic of China.
Insights
Researchers identified 36 common genes between COVID-19 and pulmonary embolism (PE). CXCL10 was found to be a key gene, potentially explaining why COVID-19 patients develop PE.
Area of Science:
- Genomics
- Immunology
- Pathogenesis
Background:
- Pulmonary embolism (PE) is a known complication of coronavirus disease 2019 (COVID-19), but the underlying mechanisms remain unclear.
- Identifying shared genetic factors could elucidate the pathogenesis of PE susceptibility in COVID-19 patients.
Purpose of the Study:
- To identify genes common to both COVID-19 and PE.
- To understand the molecular mechanisms contributing to PE development in COVID-19.
Main Methods:
- Gene expression data for COVID-19 and PE were collected from public databases.
- Common genes were identified through overlap analysis.
- Functional enrichment, protein-protein interaction, and immune infiltration analyses were performed.
- Hub genes were identified and validated in independent datasets and clinical samples.
Main Results:
- Thirty-six genes were found to be common to both COVID-19 and PE.
- Functional analyses indicated the involvement of cytokines and immune activation.
- Five hub genes were identified, including CCL2, CXCL10, ALB, EGF, and MKI67.
- CXCL10 was validated and showed significantly elevated serum levels in COVID-19 patients with and without PE compared to healthy controls.
Conclusions:
- This study identified shared genes between COVID-19 and PE, highlighting potential pathogenic pathways.
- CXCL10 is proposed as a key factor contributing to PE susceptibility in COVID-19 patients.
Background:
Although the potential of coronavirus disease 2019 (COVID-19) patients to develop pulmonary embolism (PE) is widely recognized, the underlying mechanism has not been completely elucidated. This study aimed to identify genes common to COVID-19 and PE to reveal the underlying pathogenesis of susceptibility to PE in COVID-19 patients.
Methods:
COVID-19 genes were obtained from the GEO database and the OMIM, CTD, GeneCards, and DisGeNET databases; PE genes were obtained from the OMIM, CTD, GeneCards, and DisGeNET databases. We overlapped the genes of COVID-19 and PE to obtain common genes for additional analysis, including functional enrichment, protein-protein interaction, and immune infiltration analysis. Hub genes were identified using cytoHubba, a plugin of Cytoscape, and validated using the independent datasets GSE167000 and GSE13535. The genes validated by the above datasets were further validated in clinical samples.
Results:
We obtained 36 genes shared by PE and COVID-19. Functional enrichment and immune infiltration analyses revealed the involvement of cytokines and immune activation. Five genes (CCL2, CXCL10, ALB, EGF, and MKI67) were identified as hub genes common to COVID-19 and PE. CXCL10 was validated in both independent datasets (GSE167000 and GSE13535). Serum levels of CXCL10 in the COVID-19 group and the COVID-19 combined with PE group were significantly higher than those in the healthy control group (P<0.001). In addition, there were significant differences between the COVID-19 group and the COVID-19 combined with PE group (P<0.01).
Conclusion:
Our study reveals common genes shared by PE and COVID-19 and identifies CXCL10 as a possible cause of susceptibility to PE in COVID-19 patients.
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