RPS27A as a potential clock-related diagnostic biomarker for myocardial infarction: Comprehensive bioinformatics analysis and experimental validation
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View abstract on PubMed
Summary
This summary is machine-generated.This study reveals clock genes, particularly RPS27A, are linked to Myocardial Infarction (MI). These findings highlight circadian rhythm
Area Of Science
- Cardiovascular Biology
- Chronobiology
- Molecular Genetics
Background
- Circadian system disruptions are linked to Myocardial Infarction (MI).
- Mechanisms connecting clock genes to MI pathogenesis remain unclear.
- This study investigates the role of clock genes in MI development.
Purpose Of The Study
- To identify clock genes differentially expressed in Myocardial Infarction (MI).
- To elucidate the functional pathways and biological roles of these clock genes in MI.
- To pinpoint key regulatory genes and potential therapeutic targets for MI.
Main Methods
- Analysis of MI microarray datasets (GSE151412, GSE60993) for circadian clock gene expression.
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses.
- Lasso regression for hub gene identification, validated by qRT-PCR and additional datasets.
Main Results
- Ten differentially expressed clock genes were identified in MI patients.
- Enrichment analyses implicated pathways such as Gap junction and circadian rhythm.
- RPS27A was identified as a key hub gene, with GSEA revealing links to mismatch repair and altered immune cell infiltration.
Conclusions
- The clock gene RPS27A is associated with Myocardial Infarction (MI).
- Circadian rhythm regulation by RPS27A may influence MI pathogenesis.
- Findings offer insights into MI mechanisms and potential therapeutic strategies.
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