Construction of the ceRNA network in the progression of acute myocardial infarction
Liu H., Qin S., Zhao Y., Gao L., Zhang C.
Laboratory Study on Cardiovascular Disease, published in Am J Cardiovasc Dis (2022) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Am J Cardiovasc Dis (2022)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 36743510
- PMCID
- PMC9890199
- Citations
- 2
Abstract (original English)
Acute myocardial infarction (AMI) is a common disease that induced by sudden occlusion of a coronary artery and myocardial necrosis, which causes a great medical burden worldwide. Noncoding RNAs, such as circRNA, lncRNA and miRNA, play crucial roles in the progression of cardiovascular diseases. However, the circRNA-miRNA-mRNA network in the occurrence and development of AMI needs further investigation. In this study, we downloaded three AMI datasets, including circRNA (GSE160717), miRNA (GSE24591), and mRNA (GSE66360) from GEO database. The differentially expressed candidates, and GO and KEGG functions were analyzed by RStudio, and subsequently import to PPI and Cytoscape to obtain the hub genes. By using the starbase target prediction database, we further screen the ceRNA network of circRNA-miRNA-mRNA based on the selected differentially expressed candidates. We found 46 differential expressed mRNAs, 65 miRNAs, and five circRNAs. GO functions and KEGG enrichment of the 46 mRNAs focused on immune response and functions, involving IL-17 signaling pathway, Toll-like receptor signaling pathway, cytokine-cytokine receptor interaction, TNF signaling pathway, chemokine signaling pathway, and NF-kappaB signaling pathway, which may aggravate the pathologies of AMI. PPI and Cytoscape analysis showed 10 hub genes, including TLR2, IL1B, CCL4, CCL3, CCR5, TREM1, CXCL2, NLRP3, CSF3, and CC
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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