RPS27A as a potential clock-related diagnostic biomarker for myocardial infarction: Comprehensive bioinformatics...

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.