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Updated: May 30, 2025
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Screening of biomarkers for diagnosing chronic kidney disease and heart failure with preserved ejection fraction
Can Hou1, Jiayi Xu1, Min Zhou1
1Department of Cardiovascular Medicine, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, 213000, Changzhou, Jiangsu Province, China.
Insights
This study identifies shared molecular mechanisms and three key genes (KLF4, SCD, SEL1L3) for diagnosing chronic kidney disease (CKD) and heart failure with preserved ejection fraction (HFpEF). These findings offer potential for early detection and treatment strategies.
Area of Science:
- Bioinformatics
- Genomics
- Molecular Biology
Background:
- Chronic kidney disease (CKD) and heart failure with preserved ejection fraction (HFpEF) frequently coexist.
- The precise molecular links and pathological pathways shared between CKD and HFpEF remain largely undefined.
- Understanding these shared mechanisms is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To elucidate the shared molecular mechanisms underlying the comorbidity of CKD and HFpEF.
- To identify potential diagnostic biomarkers for both conditions using bioinformatics approaches.
- To explore the roles of autophagy, ferroptosis, and immune-related processes in the pathogenesis of CKD and HFpEF.
Main Methods:
- Utilized Gene Expression Omnibus (GEO) datasets for CKD and HFpEF.
- Performed differential gene expression analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Ontology (GO) enrichment.
- Conducted weighted gene co-expression network analysis (WGCNA), correlation analyses, and constructed a miRNA-mRNA regulatory network.
Main Results:
- Identified 58 overlapping differentially expressed genes between CKD and HFpEF.
- WGCNA revealed 4086 genes associated with CKD.
- Three hub genes (KLF4, SCD, SEL1L3) were identified, linked to autophagy, ferroptosis, and immune processes, with potential diagnostic utility assessed via ROC analysis.
Conclusions:
- This research uncovers shared pathogenic pathways connecting CKD and HFpEF.
- Identified hub genes (KLF4, SCD, SEL1L3) serve as promising diagnostic markers for early detection.
- These findings pave the way for novel therapeutic interventions targeting common mechanisms in CKD and HFpEF.
Background:
Previous research has established that chronic kidney disease (CKD) and heart failure with preserved ejection fraction (HFpEF) often coexist. Although we have a preliminary understanding of the potential correlation between HFpEF and CKD, the underlying pathophysiological mechanisms remain unclear. This study aimed to elucidate the molecular mechanisms associated with CKD and HFpEF through bioinformatics analysis.
Methods:
Datasets for HFpEF and CKD were obtained from the Gene Expression Omnibus (GEO) database. The R software package "limma" was employed to conduct differential expression analysis. Functional annotation was performed using the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). We conducted weighted gene co-expression network analysis (WGCNA), correlation analysis with autophagy, ferroptosis, and immune-related processes, as well as transcriptional regulation analysis, immune infiltration analysis, and diagnostic performance evaluation. Finally, the diagnostic potential of the identified hub genes for CKD and HFpEF was assessed using ROC curve analysis (GSE37171).
Results:
Differential expression analysis revealed 58 overlapping genes, comprised of 40 up-regulated and 18 down-regulated genes. Both GO and KEGG analyses indicated enriched pathways relevant to both disorders. WGCNA identified 4086 genes associated with CKD. Further comparison with differentially expressed genes (DEGs) identified three hub genes (KLF4, SCD, and SEL1L3) that were linked to autophagy, ferroptosis, and immune processes in both conditions. Additionally, a miRNA-mRNA regulatory network involving 376 miRNAs and 12 transcription factors (TFs) was constructed. ROC curve analysis was performed to evaluate the diagnostic utility of the hub genes for CKD and HFpEF.
Conclusion:
This study elucidated shared pathogenic mechanisms and identified diagnostic markers common to both HFpEF and CKD. The identified hub genes show promise as potential tools for early diagnosis and treatment strategies for these conditions.
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