Related Experiment Video
Updated: May 5, 2026

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Coronavirus disease 2019-related myocarditis genes contribute to ECMO prognosis
An Yan1,2, Ruiying Zhang1,2, Chao Feng1,2
1Tianjin Chest Hospital, Taierzhuang North Road 261, Jinnan District, Tianjin, China.
Insights
This study identified key genes like IL6 and ITGA1 involved in COVID-19 myocarditis and ECMO treatment. These genes, expressed in various heart cells, may offer new therapeutic targets for preventing heart damage.
Area of Science:
- Cardiovascular Biology
- Immunology
- Genomics
Background:
- Coronavirus disease 2019 (COVID-19)-related myocarditis can lead to acute myocardial injury, cytokine storms, hypoxemia, and pathogen-mediated damage.
- Severe cases of COVID-19 myocarditis necessitate extracorporeal membrane oxygenation (ECMO) treatment.
- Understanding the genetic underpinnings of COVID-19 myocarditis and ECMO prognosis is crucial for developing effective therapies.
Purpose of the Study:
- To identify differentially expressed genes (DEGs) in patients with COVID-19-related myocarditis.
- To investigate the role of these DEGs in patients requiring ECMO treatment.
- To identify potential therapeutic targets for mitigating adverse cardiovascular events in COVID-19 myocarditis.
Main Methods:
- Analysis of gene expression datasets (GSE150392, GSE93101) to identify DEGs.
- Utilized Venn diagrams to find overlapping DEGs between myocarditis and ECMO cohorts.
- Performed pathway enrichment analysis, identified hub genes, and validated findings using GEO (GSE167028) and single-cell sequencing data.
Main Results:
- Identified 229 overlapping DEGs primarily involved in T cell activation, contractile actin filament bundles, and cytokine-cytokine receptor interactions.
- Screened 15 hub genes and neighboring DEGs associated with T cell activation, integrin complex, PI3K-Akt, and TNF signaling pathways.
- Validated screened genes (e.g., IL6, ITGA1, PTK2, CCL2, APOE) showing specific expression patterns in fibroblasts, cardiomyocytes, macrophages, and vascular endothelial cells.
Conclusions:
- The study identified several hub genes, including IL6, ITGA1, PTK2, and CCL2, as potential therapeutic targets for COVID-19 myocarditis.
- These validated genes, expressed in key cardiac and immune cells, may play critical roles in disease progression.
- Targeting these genes could help prevent myocardial infarction progression and adverse cardiovascular events in affected patients.
Background:
Acute myocardial injury, cytokine storms, hypoxemia and pathogen-mediated damage were the major causes responsible for mortality induced by coronavirus disease 2019 (COVID-19)-related myocarditis. These need ECMO treatment. We investigated differentially expressed genes (DEGs) in patients with COVID-19-related myocarditis and ECMO prognosis.
Methods:
GSE150392 and GSE93101 were analyzed to identify DEGs. A Venn diagram was used to obtain the same transcripts between myocarditis-related and ECMO-related DEGs. Enrichment pathway analysis was performed and hub genes were identified. Pivotal miRNAs, transcription factors, and chemicals with the screened gene interactions were identified. The GSE167028 dataset and single-cell sequencing data were used to validate the screened genes.
Results:
Using a Venn diagram, 229 overlapping DEGs were identified between myocarditis-related and ECMO-related DEGs, which were mainly involved in T cell activation, contractile actin filament bundle, actomyosin, cyclic nucleotide phosphodiesterase activity, and cytokine-cytokine receptor interaction. 15 hub genes and 15 neighboring DEGs were screened, which were mainly involved in the positive regulation of T cell activation, integrin complex, integrin binding, the PI3K-Akt signaling pathway, and the TNF signaling pathway. Data in GSE167028 and single-cell sequencing data were used to validate the screened genes, and this demonstrated that the screened genes CCL2, APOE, ITGB8, LAMC2, COL6A3 and TNC were mainly expressed in fibroblast cells; IL6, ITGA1, PTK2, ITGB5, IL15, LAMA4, CAV1, SNCA, BDNF, ACTA2, CD70, MYL9, DPP4, ENO2 and VEGFC were expressed in cardiomyocytes; IL6, PTK2, ITGB5, IL15, APOE, JUN, SNCA, CD83, DPP4 and ENO2 were expressed in macrophages; and IL6, ITGA1, PTK2, ITGB5, IL15, VCAM1, LAMA4, CAV1, ACTA2, MYL9, CD83, DPP4, ENO2, VEGFC and IL32 were expressed in vascular endothelial cells.
Conclusion:
The screened hub genes, IL6, ITGA1, PTK2, ITGB3, ITGB5, CCL2, IL15, VCAM1, GZMB, APOE, ITGB8, LAMA4, LAMC2, COL6A3 and TNFRSF9, were validated using GEO dataset and single-cell sequencing data, which may be therapeutic targets patients with myocarditis to prevent MI progression and adverse cardiovascular events.
More Related Videos
10:18Generation and Characterization of Right Ventricular Myocardial Infarction Induced by Permanent Ligation of the Right Coronary Artery in Mice
Published on: February 1, 2022
03:45Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
Published on: August 8, 2022
Related Concept Videos
Myocarditis I: Introduction
Myocarditis III: Medical Management
Cardiomyopathy I: Introduction and Classification
Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy IV: Restrictive Cardiomyopathy