ArticleMolecular medicine reports2018
Identification and functional analysis of differentially expressed genes associated with cerebral ischemia/reperfusion injury through bioinformatics methods.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Evaluation of the serum level of Lipocalin 2 in vitiligo.Archives of dermatological research · 2025Article
- Lipocalin-2 and Cerebral Stroke.Frontiers in molecular neuroscience · 2022Review
- Tackling Ischemic Reperfusion Injury With the Aid of Stem Cells and Tissue Engineering.Frontiers in physiology · 2021Review
- Neutralization of Lipocalin-2 Diminishes Stroke-Reperfusion Injury.International journal of molecular sciences · 2020Article
- Lidocaine improves cerebral ischemia-reperfusion injury in rats through cAMP/PKA signaling pathway.Experimental and therapeutic medicine · 2020Article
- Four Immune-Related Long Non-coding RNAs for Prognosis Prediction in Patients With Hepatocellular Carcinoma.Frontiers in molecular biosciences · 2020Article
- Identification of key transcription factors associated with cerebral ischemia‑reperfusion injury based on gene‑set enrichment analysis.International journal of molecular medicine · 2019Article
- The Role of Mast Cells in Stroke.Cells · 2019Review
- MicroRNA-429/Cxcl1 Axis Protective Against Oxygen Glucose Deprivation/Reoxygenation-Induced Injury in Brain Microvascular Endothelial Cells.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia/reperfusion (I/R) injury results in detrimental complications. However, little is known about the underlying molecular mechanisms involved in the reperfusion stage. The aim of the present study was to identify a gene expression profile associated with cerebral ischemia/reperfusion injury. The GSE23160 dataset, which comprised data from sham control samples and post‑I/R injury brain tissues that were obtained using a middle cerebral artery occlusion (MCAO) model at 2, 8 and 24 h post‑reperfusion, was downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) in the MCAO samples compared with controls were screened using the GEO2R web tool. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis for DEGs was performed using the online tool DAVID. Furthermore, a protein‑protein interaction (PPI) network was constructed using the STRING database and Cytoscape software. In total, 32 DEGs at 2 h post‑reperfusion, 39 DEGs at 8 h post‑reperfusion and 91 DEGs at 24 h post‑reperfusion were identified, while 15 DEGs were common among all three groups. GO analysis revealed that the DEGs at all three time‑points were enriched in 'chemotaxis' and 'inflammatory response' terms, while KEGG pathway analysis demonstrated that DEGs were significantly enriched in the 'chemokine signaling pathway'. Furthermore, following PPI network construction, Cxcl1 was identified as the only hub gene that was common among all three time‑points. In conclusion, the present study has demonstrated a global view of the potential molecular differences following cerebral I/R injury and may contribute to an improved understanding of the reperfusion stage, which may ultimately aid in the development of future clinical strategies.
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