Identification of hub genes and enriched pathways in renal ischemia–reperfusion injury via integrative transcriptomic and network analysis

Perçin Pazarcı; Gülşah Evyapan

Makale detayları

Identification of hub genes and enriched pathways in renal ischemia–reperfusion injury via integrative transcriptomic and network analysis

Yazarlar:

Perçin Pazarcı | Gülşah Evyapan

Yayıncı:

MediHealth Academy Yayıncılık

Ana Başlıklar:

Nefroloji | Tıbbi Genetik (Kanser Genetiği hariç)

Dergi:

Anatolian Current Medical Journal Vol.7 Issue 4, pp.459-464

Belge Tipi:

Makale

Yayın Tarihi:

7/2025

Belge Dili:

İngilizce

Document ID (Org No.):

2001355609

pISSN:

2718-0115

Anahtar kelimeler:

Özet:

 Aims: This study aimed to identify key genes and pathways involved in the pathogenesis of renal ischemiareperfusion injury IRI-induced acute kidney injury AKI using an integrative bioinformatics approach. Methods: Publicly available gene expression profiles from two independent rat kidney microarray datasets GSE27274 and GSE58438 were analyzed to identify differentially expressed genes DEGs between IRI and control groups. DEGs with an adjusted p-value 0.05 and log2 fold change 1 were considered significant. Common DEGs from both datasets were subjected to Gene Ontology GO and Kyoto Encyclopedia of Genes and Genomes KEGG enrichment analyses. Proteinprotein interaction networks were constructed using STRING and cytoscape, and hub genes were identified with the maximal clique centrality algorithm via the CytoHubba plugin. Results: A total of 189 overlapping DEGs were identified 117 upregulated, 72 downregulated. Upregulated DEGs were enriched in pathways associated with glutathione metabolism and oxidative stress response, while downregulated DEGs were associated with DNA replication and inflammatory signaling. Hub genes for upregulated DEGs included Gclc, Gclm, Anpep, and Gss, while downregulated hub genes included Mcm2, Gins1, Pcna, and Tnf. These genes represent potential regulatory nodes in the renal IRI response. Conclusion: This study highlights redox regulation, amino acid metabolism, immune modulation, and cell cycle arrest as major components in the molecular pathogenesis of renal IRI. The identified hub genes may serve as potential diagnostic biomarkers and therapeutic targets. These findings provide a framework for future experimental validation and drug development efforts in AKI caused by IRI.

 Aims: This study aimed to identify key genes and pathways involved in the pathogenesis of renal ischemiareperfusion injury IRI-induced acute kidney injury AKI using an integrative bioinformatics approach. Methods: Publicly available gene expression profiles from two independent rat kidney microarray datasets GSE27274 and GSE58438 were analyzed to identify differentially expressed genes DEGs between IRI and control groups. DEGs with an adjusted p-value 0.05 and log2 fold change 1 were considered significant. Common DEGs from both datasets were subjected to Gene Ontology GO and Kyoto Encyclopedia of Genes and Genomes KEGG enrichment analyses. Proteinprotein interaction networks were constructed using STRING and cytoscape, and hub genes were identified with the maximal clique centrality algorithm via the CytoHubba plugin. Results: A total of 189 overlapping DEGs were identified 117 upregulated, 72 downregulated. Upregulated DEGs were enriched in pathways associated with glutathione metabolism and oxidative stress response, while downregulated DEGs were associated with DNA replication and inflammatory signaling. Hub genes for upregulated DEGs included Gclc, Gclm, Anpep, and Gss, while downregulated hub genes included Mcm2, Gins1, Pcna, and Tnf. These genes represent potential regulatory nodes in the renal IRI response. Conclusion: This study highlights redox regulation, amino acid metabolism, immune modulation, and cell cycle arrest as major components in the molecular pathogenesis of renal IRI. The identified hub genes may serve as potential diagnostic biomarkers and therapeutic targets. These findings provide a framework for future experimental validation and drug development efforts in AKI caused by IRI.

 Aims: This study aimed to identify key genes and pathways involved in the pathogenesis of renal ischemiareperfusion injury IRI-induced acute kidney injury AKI using an integrative bioinformatics approach. Methods: Publicly available gene expression profiles from two independent rat kidney microarray datasets GSE27274 and GSE58438 were analyzed to identify differentially expressed genes DEGs between IRI and control groups. DEGs with an adjusted p-value 0.05 and log2 fold change 1 were considered significant. Common DEGs from both datasets were subjected to Gene Ontology GO and Kyoto Encyclopedia of Genes and Genomes KEGG enrichment analyses. Proteinprotein interaction networks were constructed using STRING and cytoscape, and hub genes were identified with the maximal clique centrality algorithm via the CytoHubba plugin. Results: A total of 189 overlapping DEGs were identified 117 upregulated, 72 downregulated. Upregulated DEGs were enriched in pathways associated with glutathione metabolism and oxidative stress response, while downregulated DEGs were associated with DNA replication and inflammatory signaling. Hub genes for upregulated DEGs included Gclc, Gclm, Anpep, and Gss, while downregulated hub genes included Mcm2, Gins1, Pcna, and Tnf. These genes represent potential regulatory nodes in the renal IRI response. Conclusion: This study highlights redox regulation, amino acid metabolism, immune modulation, and cell cycle arrest as major components in the molecular pathogenesis of renal IRI. The identified hub genes may serve as potential diagnostic biomarkers and therapeutic targets. These findings provide a framework for future experimental validation and drug development efforts in AKI caused by IRI.

 Aims: This study aimed to identify key genes and pathways involved in the pathogenesis of renal ischemiareperfusion injury IRI-induced acute kidney injury AKI using an integrative bioinformatics approach. Methods: Publicly available gene expression profiles from two independent rat kidney microarray datasets GSE27274 and GSE58438 were analyzed to identify differentially expressed genes DEGs between IRI and control groups. DEGs with an adjusted p-value 0.05 and log2 fold change 1 were considered significant. Common DEGs from both datasets were subjected to Gene Ontology GO and Kyoto Encyclopedia of Genes and Genomes KEGG enrichment analyses. Proteinprotein interaction networks were constructed using STRING and cytoscape, and hub genes were identified with the maximal clique centrality algorithm via the CytoHubba plugin. Results: A total of 189 overlapping DEGs were identified 117 upregulated, 72 downregulated. Upregulated DEGs were enriched in pathways associated with glutathione metabolism and oxidative stress response, while downregulated DEGs were associated with DNA replication and inflammatory signaling. Hub genes for upregulated DEGs included Gclc, Gclm, Anpep, and Gss, while downregulated hub genes included Mcm2, Gins1, Pcna, and Tnf. These genes represent potential regulatory nodes in the renal IRI response. Conclusion: This study highlights redox regulation, amino acid metabolism, immune modulation, and cell cycle arrest as major components in the molecular pathogenesis of renal IRI. The identified hub genes may serve as potential diagnostic biomarkers and therapeutic targets. These findings provide a framework for future experimental validation and drug development efforts in AKI caused by IRI.

Makale detayları

Identification of hub genes and enriched pathways in renal ischemia–reperfusion injury via integrative transcriptomic and network analysis

Yazarlar:

Perçin Pazarcı | Gülşah Evyapan

Yayıncı:

MediHealth Academy Yayıncılık

Ana Başlıklar:

Nefroloji | Tıbbi Genetik (Kanser Genetiği hariç)

Dergi:

Anatolian Current Medical Journal Vol.7 Issue 4, pp.459-464

Belge Tipi:

Makale

Yayın Tarihi:

7/2025

Belge Dili:

İngilizce

Document ID (Org No.):

2001355609

pISSN:

2718-0115

Acute kidney injury

ischemia-reperfusion injury

hub genes

oxidative stress

bioinformaticsAcute kidney injury

ischemia-reperfusion injury

hub genes

oxidative stress

bioinformatics

Sayı

Makale detayları

Yazarlar: Perçin Pazarcı | Gülşah Evyapan

Yayıncı: MediHealth Academy Yayıncılık

Ana Başlıklar: Nefroloji | Tıbbi Genetik (Kanser Genetiği hariç)

Dergi: Anatolian Current Medical Journal Vol.7 Issue 4, pp.459-464

Belge Tipi: Makale

Yayın Tarihi: 7/2025

Belge Dili: İngilizce

Document ID (Org No.): 2001355609

pISSN: 2718-0115

Sayı

Yazarlar:

Perçin Pazarcı | Gülşah Evyapan

Yayıncı:

MediHealth Academy Yayıncılık

Ana Başlıklar:

Nefroloji | Tıbbi Genetik (Kanser Genetiği hariç)

Dergi:

Anatolian Current Medical Journal Vol.7 Issue 4, pp.459-464

Belge Tipi:

Makale

Yayın Tarihi:

7/2025

Belge Dili:

İngilizce

Document ID (Org No.):

2001355609

pISSN:

2718-0115