Crosstalk between Circulatory Microenvironment and Vascular Endothelial Cells in Acute Myocardial Infarction
Beiyou Lin1, Weiwei Zheng2, Xiaofei Jiang1
1Department of Cardiology, Zhuhai People's Hospital, (Zhuhai hospital affiliated with Jinan University), Zhuhai, Guangdong, 519000, People's Republic of China.
Insights
Researchers explored cell and molecular mechanisms of acute myocardial infarction (AMI). They identified common differentially expressed genes (DEGs) and cell-cell interactions, revealing potential biomarkers and therapeutic targets for AMI.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genomics
Background:
- Acute myocardial infarction (AMI) has high mortality due to incompletely understood cellular and molecular mechanisms.
- Exploring cell crosstalk and molecular pathways is crucial for understanding AMI pathogenesis.
Purpose of the Study:
- To investigate the cellular and molecular mechanisms underlying acute myocardial infarction (AMI).
- To identify potential biomarkers and therapeutic targets by analyzing gene expression and cell interactions in AMI.
Main Methods:
- Differential gene expression (DEGs) analysis was performed on peripheral blood, endothelial, platelets, and mononuclear cells.
- Gene set enrichment analysis (GSEA) explored functional pathways of DEGs.
- Crosstalk and pivot analysis identified cell-cell interactions and potential molecular mechanisms involving exosome lncRNA.
Main Results:
- Eleven common differentially expressed genes (CDEGs) were identified as potential diagnostic biomarkers for AMI.
- Significant cell crosstalk was observed among intravascular cells and peripheral blood.
- A cell-cell interaction map regulated by exosome lncRNA was constructed, highlighting its role in AMI development.
- Eight hub genes were identified as potential biomarkers for AMI.
Conclusions:
- The study provides insights into the cellular and molecular mechanisms of AMI.
- Identified biomarkers and pathways can guide future research and the development of novel therapies for AMI.
Background:
The reason of high mortality of acute myocardial infarction (AMI) was the lack of exploring the cellular and molecular mechanism of AMI. Therefore, we explored the crosstalk among cells, as well as its potential molecular mechanism of mediating AMI.
Methods:
The gene expression profile of peripheral blood, endothelial, platelets and mononuclear cells were applied to differentially expressed genes (DEGs) analysis. ClusterProfiler and the package of gene set enrichment analysis (GSEA) were applied to explore the potential functional pathways of DEGs in 3 types of intravascular cells (endothelial, platelets and mononuclear cells) and peripheral blood. Subsequently, we extracted the surface receptors, secreted proteins and extracellular matrix from the up-regulated DEGs to explore their potential interactions mechanism of AMI by crosstalk and pivot analysis.
Findings:
A total 11 common regulated DEGs (CDEGs) were identified, which might be potential biomarkers for AMI diagnosis. The abnormal pathways involved in DEGs of 3 types of intravascular cells and peripheral blood were shown, which also verified by GSEA. Afterwards, it was found that there was crosstalk in 3 types of intravascular cells and peripheral blood. Furthermore, we constructed a cell-cell interaction map among cells in AMI regulated by exosome lncRNA, which was involved in the development of AMI. Finally, we identified 8 hub genes, which might be potential biomarkers of AMI.
Interpretation:
The result of this study can not only be used as a reference for subsequent experiments and further exploration, but also contribute to the development of novel cell and molecular therapies.
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