RPS27A as a potential clock-related diagnostic biomarker for myocardial infarction: Comprehensive bioinformatics analysis and experimental validation

TL;DR

This study identifies RPS27A as a potential biomarker for diagnosing heart attacks by analyzing circadian genes and their role in heart disease.

Contribution

The study introduces RPS27A as a novel clock-related biomarker for myocardial infarction, validated through bioinformatics and experimental methods.

Findings

RPS27A was confirmed as a key gene in myocardial infarction via Lasso regression and qRT-PCR.

Clock genes are linked to MI through pathways like gap junction and circadian rhythm.

Immune infiltration analysis showed differences in B-cell and CD4+ T-cell populations in MI patients.

Abstract

•Clock genes are linked to myocardial infarction, offering novel insights into its pathogenesis.•Ten differentially expressed clock genes suggest new pathways in myocardial infarction development.•RPS27A’s core role in myocardial infarction was validated via Lasso regression and qRT-PCR, showing elevated expression.•Gene enrichment analysis uncovers gap junction and circadian rhythm pathways in myocardial infarction.•RPS27A was identified as a potential molecular target for diagnosing myocardial infarction.

Clock genes are linked to myocardial infarction, offering novel insights into its pathogenesis.

Ten differentially expressed clock genes suggest new pathways in myocardial infarction development.

RPS27A’s core role in myocardial infarction was validated via Lasso regression and qRT-PCR, showing elevated expression.

Gene enrichment analysis uncovers gap junction and circadian rhythm pathways in myocardial infarction.

RPS27A was identified as a potential molecular target for diagnosing myocardial infarction.

The circadian system plays a crucial role in managing cardiovascular functions, with disturbances in this system associated with Myocardial Infarction (MI). Despite this connection, the exact mechanisms by which clock genes influence MI occurrence are not well-defined. This research focused on investigating the link between clock genes and MI.

The authors examined MI microarray datasets (GSE151412 and GSE60993) from the GEO database, concentrating on Differentially Expressed Genes (DEGs) associated with the circadian system. To clarify critical biological functions and pathways, the authors performed enrichment analyses using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). Through Lasso regression, the authors pinpointed hub genes and confirmed their relevance using both the GSE66360 dataset and quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Furthermore, the authors conducted single-Gene Set Enrichment Analysis (GSEA) to reveal pathways linked to the hub gene. The analysis extended to exploring drug interactions and networks involving competing endogenous RNA (ceRNA).

The present analysis identified ten clock genes associated with circadian rhythms that showed differential expression between MI patients and healthy controls. Enrichment analysis suggested these genes’ roles in pathways like the Gap junction and circadian rhythm pathways. Following Lasso regression and validation, RPS27A was identified as the main hub gene. GSEA further highlighted enriched pathways, such as mismatch repair. Additionally, immune infiltration analysis revealed notable differences in B-cell and CD4+ T-cell populations between the MI group and the control group.

The present findings suggest that the clock-related gene RPS27A is associated with MI, potentially influencing its development through circadian rhythm regulation. These results enhance the understanding of MI pathogenesis and may offer new avenues for therapeutic intervention.

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