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Published on: September 20, 2024
Exploring Potential Biomarkers and Molecular Mechanisms of Ischemic Cardiomyopathy and COVID-19 Comorbidity Based on
Simin Luo1,2, Xuan Zhang2, Xiang Xiao2
1School of Basic Medical Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.
Insights
This study identifies key genes (HSP90AA1, HSPA9, SRSF1) linked to ischemic cardiomyopathy (ICM) and COVID-19 co-pathogenesis, suggesting a role for angiogenesis. Potential therapeutic drugs were also predicted.
Area of Science:
- Molecular Biology
- Genomics
- Cardiology
Background:
- COVID-19 (SARS-CoV-2) significantly worsens outcomes for patients with cardiovascular complications.
- The shared molecular mechanisms underlying ischemic cardiomyopathy (ICM) and COVID-19 remain largely unknown.
Purpose of the Study:
- To investigate the molecular mechanisms and identify biomarkers for the co-pathogenesis of ICM and COVID-19.
- To explore potential therapeutic targets for this comorbidity.
Main Methods:
- Differential gene expression analysis of ICM and COVID-19 datasets (GSE5406, GSE164805) using GEO2R.
- Enrichment analysis, protein-protein interaction network construction, and hub gene screening.
- Validation of diagnostic performance using external datasets (GSE116250, GSE211979) and ROC curves.
- Construction of transcription factor and microRNA regulatory networks.
- Drug prediction and molecular docking validation via cMAP.
Main Results:
- Identified 81 common differentially expressed genes (DEGs) between ICM and COVID-19, with enrichment in angiogenesis-related pathways.
- Screened three key hub genes: HSP90AA1, HSPA9, and SRSF1, demonstrating high diagnostic performance (AUC > 0.7) across four datasets.
- Established co-regulation of these hub genes by miR-16-5p and KLF9.
- Predicted vindesine and ON-01910 as potential therapeutic agents with favorable binding affinities.
Conclusions:
- HSP90AA1, HSPA9, and SRSF1 are identified as potential biomarkers for the co-pathogenesis of ICM and COVID-19.
- Angiogenesis may play a crucial role in the shared disease mechanisms.
- Vindesine and ON-01910 show promise as therapeutic interventions for managing this comorbidity.
Abstract:
Cardiovascular complications combined with COVID-19 (SARS-CoV-2) lead to a poor prognosis in patients. The common pathogenesis of ischemic cardiomyopathy (ICM) and COVID-19 is still unclear. Here, we explored potential molecular mechanisms and biomarkers for ICM and COVID-19. Common differentially expressed genes (DEGs) of ICM (GSE5406) and COVID-19 (GSE164805) were identified using GEO2R. We performed enrichment and protein-protein interaction analyses and screened key genes. To confirm the diagnostic performance for these hub genes, we used external datasets (GSE116250 and GSE211979) and plotted ROC curves. Transcription factor and microRNA regulatory networks were constructed for the validated hub genes. Finally, drug prediction and molecular docking validation were performed using cMAP. We identified 81 common DEGs, many of which were enriched in terms of their relation to angiogenesis. Three DEGs were identified as key hub genes (HSP90AA1, HSPA9, and SRSF1) in the protein-protein interaction analysis. These hub genes had high diagnostic performance in the four datasets (AUC > 0.7). Mir-16-5p and KLF9 transcription factor co-regulated these hub genes. The drugs vindesine and ON-01910 showed good binding performance to the hub genes. We identified HSP90AA1, HSPA9, and SRSF1 as markers for the co-pathogenesis of ICM and COVID-19, and showed that co-pathogenesis of ICM and COVID-19 may be related to angiogenesis. Vindesine and ON-01910 were predicted as potential therapeutic agents. Our findings will contribute to a deeper understanding of the comorbidity of ICM with COVID-19.
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