ArticleJournal of inflammation research2023
CXCL10 May Be Responsible for Susceptibility to Pulmonary Embolism in COVID-19 Patients.
Article in Journal of inflammation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Serum cytokine profiling reveals CXCL10 (IP-10) as a major predictor of severe COVID-19 outcomes in hospitalized patients during the first pandemic wave in Italy.Frontiers in immunology · 2026Article
- Integration of angiogenesis and programmed cell death mechanisms unveils potential diagnostic and therapeutic targets in spinal cord injury.Journal of translational medicine · 2025Article
- Determination of key hub genes in Leishmaniasis as potential factors in diagnosis and treatment based on a bioinformatics study.Scientific reports · 2024Article
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Authors and funding
7 authors.
Funding
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Abstract
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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