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Updated: Jun 23, 2025

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
Published on: May 24, 2020
Bioinformatics analysis of potential common pathogenic mechanisms for COVID-19 and venous thromboembolism
Ling Zhang1, Jing Qin1, Peiwu Li1
1Department of Emergency Medicine, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
Insights
Patients with coronavirus disease 2019 (COVID-19) face higher venous thromboembolism (VTE) risks. This study identified common molecular pathways and eight key genes, offering insights into VTE and COVID-19 pathogenesis.
Area of Science:
- Molecular biology
- Genomics
- Bioinformatics
Background:
- Coronavirus disease 2019 (COVID-19) patients exhibit elevated venous thromboembolism (VTE) rates.
- The precise molecular mechanisms linking COVID-19 and VTE remain unclear.
- Further investigation into these molecular underpinnings is crucial.
Purpose of the Study:
- To elucidate the molecular mechanisms shared between COVID-19 and VTE.
- To identify common differentially expressed genes (DEGs) and regulatory networks.
- To explore potential diagnostic markers for both conditions.
Main Methods:
- Downloaded and analyzed gene expression profiles for COVID-19 and VTE from the GEO database.
- Identified common DEGs, performed functional annotation, and constructed protein-protein interaction (PPI) networks.
- Built transcription factor (TF)-gene and TF-miRNA regulatory networks for hub genes.
Main Results:
- Identified 42 common DEGs between COVID-19 and VTE.
- Functional analyses revealed shared biological functions and signaling pathways.
- Discovered 8 significant hub genes (RSL24D1, RPS17, RPS27, HINT1, COX7C, RPL35, RPL34, NDUFA4) with diagnostic potential.
Conclusions:
- The study highlights common pathogenic pathways in COVID-19 and VTE.
- Identified pivotal genes may serve as novel targets for mechanistic research.
- Findings offer new perspectives for understanding and potentially treating these interconnected conditions.
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.
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