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Published on: January 28, 2020
Exploring potential biomarkers and therapeutic targets of long COVID-associated inflammatory cardiomyopathy
Peng Qi1, Mengjie Huang2, Haiyan Zhu1
1Department of Emergency, First Medical Center of Chinese PLA General Hospital, Beijing, China.
Insights
Long COVID can cause inflammatory cardiomyopathy, but its cause is unknown. This study identified key genes (VEGFA, FOXO1, CXCR4, SMAD4, KRAS, TXN) suggesting an immune response, not viral infection, drives this condition.
Area of Science:
- Cardiovascular Research
- Infectious Disease Epidemiology
- Molecular Biology
Background:
- Long COVID significantly impacts social life and health, with confirmed cardiovascular disease risks.
- The specific pathogenesis of long COVID-associated inflammatory cardiomyopathy remains unclear.
- Understanding this condition is crucial for developing effective treatments.
Purpose of the Study:
- To explore potential biomarkers for long COVID-associated inflammatory cardiomyopathy.
- To identify novel therapeutic targets for this condition.
- To elucidate the underlying molecular mechanisms.
Main Methods:
- Utilized Gene Expression Omnibus (GEO) datasets for differentially expressed genes (DEGs).
- Performed functional enrichment analysis and constructed a protein-protein interaction (PPI) network.
- Identified and validated hub genes using independent datasets.
Main Results:
- Identified 3,098 upregulated and 1965 downregulated DEGs in inflammatory cardiomyopathy datasets.
- Confirmed VEGFA, FOXO1, CXCR4, SMAD4 as upregulated hub genes and KRAS, TXN as downregulated hub genes.
- Validation suggested immune-mediated response and inflammation, not direct viral infection, as the primary cause.
Conclusions:
- Identified potential biomarkers and therapeutic targets for long COVID-associated inflammatory cardiomyopathy.
- Findings offer new insights into the pathogenesis of this condition.
- Further clinical studies are warranted due to the severe impact of long COVID.
Background:
The negative impact of long COVID on social life and human health is increasingly prominent, and the elevated risk of cardiovascular disease in patients recovering from COVID-19 has also been fully confirmed. However, the pathogenesis of long COVID-related inflammatory cardiomyopathy is still unclear. Here, we explore potential biomarkers and therapeutic targets of long COVID-associated inflammatory cardiomyopathy.
Methods:
Datasets that met the study requirements were identified in Gene Expression Omnibus (GEO), and differentially expressed genes (DEGs) were obtained by the algorithm. Then, functional enrichment analysis was performed to explore the basic molecular mechanisms and biological processes associated with DEGs. A protein-protein interaction (PPI) network was constructed and analyzed to identify hub genes among the common DEGs. Finally, a third dataset was introduced for validation.
Results:
Ultimately, 3,098 upregulated DEGs and 1965 downregulated DEGs were extracted from the inflammatory cardiomyopathy dataset. A total of 89 upregulated DEGs and 217 downregulated DEGs were extracted from the dataset of convalescent COVID patients. Enrichment analysis and construction of the PPI network confirmed VEGFA, FOXO1, CXCR4, and SMAD4 as upregulated hub genes and KRAS and TXN as downregulated hub genes. The separate dataset of patients with COVID-19 infection used for verification led to speculation that long COVID-associated inflammatory cardiomyopathy is mainly attributable to the immune-mediated response and inflammation rather than to direct infection of cells by the virus.
Conclusion:
Screening of potential biomarkers and therapeutic targets sheds new light on the pathogenesis of long COVID-associated inflammatory cardiomyopathy as well as potential therapeutic approaches. Further clinical studies are needed to explore these possibilities in light of the increasingly severe negative impacts of long COVID.
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