ArticleFrontiers in immunology2025
Identification of diagnostic genes for myocardial ischemia reperfusion injury associated with metabolic syndrome through the integration of bioinformatics analysis, molecular docking and experimental validation.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- MITF Regulates CFTR Expression to Participate in Myocardial Ischemia-Reperfusion Injury.The journal of gene medicine · 2026Article
- Potential Relationship Between YTHDF3 and CFTR in Myocardial Ischemia-Reperfusion Injury.Journal of cellular and molecular medicine · 2026Article
- The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming.Frontiers in immunology · 2026Review
- Identification of LncRNA Mhrt as a potential biomarker for preventing the progression of Myocardial Ischemia-Reperfusion Injury through bioinformatics and experimental validation.BMC cardiovascular disorders · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Metabolic dysregulation in metabolic syndrome (MetS) exacerbates myocardial ischemia-reperfusion injury (MIRI). This study aimed to identify diagnostic biomarkers and therapeutic candidates for MetS-associated MIRI. Methods: Three MIRI and two MetS datasets from GEO were analyzed using differential expression analysis, WGCNA, and machine learning (LASSO/SVM-RFE). Hub genes were validated via qRT-PCR in hypoxia-induced H9C2 cells. Drug candidates were predicted via PPI networks, CTD, and molecular docking, followed by experimental evaluation of dexamethasone. Results: Five hub genes-DAK, GTF3C5, KCNMB1, TRAF1, and ZNF692-were identified, with distinct expression patterns (DAK/GTF3C5 downregulated; KCNMB1/TRAF1/ZNF692 upregulated). These genes were enriched in immune-related pathways, and their diagnostic performance was robust (AUCs: 0.875-0.969). Dexamethasone downregulated KCNMB1/TRAF1/ZNF692 and reduced apoptosis in H9C2 cells. Conclusion: This study reveals immune-metabolic dysregulation as a key driver of MetS-MIRI, proposes five biomarkers for diagnosis, and highlights dexamethasone as a promising therapeutic candidate.
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