ArticleJournal of inflammation research2021
Crosstalk between Circulatory Microenvironment and Vascular Endothelial Cells in Acute Myocardial Infarction.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Identification of lipid metabolism-related genes in myocardial infarction: implications for diagnosis and therapy.Journal of cardiothoracic surgery · 2025Article
- Identification of Potential Crucial Biomarkers in STEMI Through Integrated Bioinformatic Analysis.Arquivos brasileiros de cardiologia · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe 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.
methodsThe 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.
findingsA 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.
interpretationThe 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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Registered trials
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