ArticleInternational journal of molecular medicine2019
Identification of key transcription factors associated with cerebral ischemia‑reperfusion injury based on gene‑set enrichment analysis.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Geniposide protects against cerebral ischemic injury by targeting SOX2/RIPK1 axis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Immunological Mechanisms and Therapeutic Strategies in Cerebral Ischemia-Reperfusion Injury: From Inflammatory Response to Neurorepair.International journal of molecular sciences · 2025Review
- Novel insights into immunopathogenesis and crucial biomarkers between primary open-angle glaucoma and systemic lupus erythematosus.iMetaOmics · 2024Article
- Role of transcription factors, noncoding RNAs, epitranscriptomics, and epigenetics in post-ischemic neuroinflammation.Journal of neurochemistry · 2024Review
- Genome-wide identification analysis in wild-typeFrontiers in genetics · 2024Article
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- Gli2-induced lncRNA Peg13 alleviates cerebral ischemia-reperfusion injury by suppressing Yy1 transcription in a PRC2 complex-dependent manner.Metabolic brain disease · 2023Article
- Neuroglia Cells Transcriptomic in Brain Development, Aging and Neurodegenerative Diseases.Aging and disease · 2023Review
- The new insight into the inflammatory response following focused ultrasound-mediated blood-brain barrier disruption.Fluids and barriers of the CNS · 2022Article
- Cell Heterogeneity Uncovered by Single-Cell RNA Sequencing Offers Potential Therapeutic Targets for Ischemic Stroke.Aging and disease · 2022Review
- Single-cell RNA-seq reveals the transcriptional landscape in ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Upregulation of SPI1 during myocardial infarction aggravates cardiac tissue injury and disease progression through activation of the TLR4/NFκB axis.American journal of translational research · 2022Article
- Peroxisome Proliferator-Activated Receptor-Gamma (PPAR-ɣ): Molecular Effects and Its Importance as a Novel Therapeutic Target for Cerebral Ischemic Injury.Neurochemical research · 2021Review
- The Impact of Juvenile Microglia Transcriptomics on the Adult Brain Regeneration after Cerebral Ischemia.Current health sciences journalArticle
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia‑reperfusion injury (CIRI) usually causes detrimental complications following reperfusion therapy in stroke patients. The present study systematically investigated the regulatory mechanism involved in the pathogenesis of CIRI using gene set enrichment analysis of the transient middle cerebral artery occlusion mouse stroke model. The results revealed a total of 13 CIRI‑related transcription factors (TFs), including CCAAT enhancer binding protein b (Cebpb), Cebpa, early growth response‑1, Fos, Rela, Jund, signal transduction and activator of transcription 5a/b, transformation related protein 53, GLI family zinc finger 2 (Gli2), Sp3, TF AP‑2 α (Tfap2a) and spleen focus forming virus proviral integration oncogene (Spi1). To the best of our knowledge, five TFs (Cebpa, Gli2, Sp3, Tfap2a and Spi1) were the first to be reported associated with CIRI in the present study. The five novel CIRI‑related TFs were mainly associated with pathways of inflammation and responses to reperfusion, including the tumor necrosis factor signaling pathway (Gli2, Spi1 and Tfap2a, P=0.0035, 0.0035 and 0.048, respectively), interleuking‑17 signaling pathway (Cebpa, Gli2, Sp3, Spi1 and Tfap2a, P=0.019, 0.047, 0.019, 0.035 and 0.005, respectively) and fluid shear stress and atherosclerosis (Gli2, Sp3, Spi1 and Tfap2a, P=0.047, 0.046, 0.013 and 0.003, respectively). These results may improve understanding of the potential molecular mechanism underlying the pathogenesis of CIRI at the genome‑wide level.
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