ArticleHereditas2025
Identification of regulator gene and pathway in myocardial ischemia-reperfusion injury: a bioinformatics and biological validation study.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
- Rosa davurica Pall. as a Functional Food in Ameliorating Acute Myocardial Ischemia: An Integrated Multi-Omics Study on TNF-α and Oxidative Stress.Chemistry & biodiversity · 2026Article
- Network Pharmacology Approaches to Myocardial Infarction Reperfusion Injury: Exploring Mechanisms, Pathophysiology, and Novel Therapies.Biomedicines · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundAcute myocardial infarction (AMI) is the primary cause of cardiac mortality worldwide. However, myocardial ischemia-reperfusion injury (MIRI) following reperfusion therapy is common in AMI, causing myocardial damage and affecting the patient's prognosis. Presently, there are no effective treatments available for MIRI.
methodsWe performed a comprehensive bioinformatics analysis using three GEO datasets on differentially expressed genes, including gene ontology (GO), pathway enrichment analyses, and protein-protein interaction (PPI) network analysis. Cytoscape and LASSO methods were employed to identify novel regulator genes for ischemia-reperfusion (I/R). Notably, gene S100A9 was identified as a potential regulator of I/R. Additionally, clinical sample datasets were analyzed to prove the expression and mechanism of S100A9 and its down genes in I/R. The correlation of S100A9 with cardiac events was also examined to enhance the reliability of our results.
resultsWe identified 135 differential genes between the peripheral blood of 47 controls and 92 I/R patients. S100A9 was distinguished as a novel regulator gene of I/R with diagnostic potential. RT-qPCR test demonstrated significant upregulation of S100A9 in I/R. We also verified that S100A9 expression strongly correlates with left ventricular ejection fraction (LVEF) and MIRI.
conclusionThis study confirms that S100A9 is a key regulator of I/R progression and may participate in ischemia-reperfusion injury by upregulating RAGE /NFKB-NLRP3 activation. Elevated S100A9 levels may serve as a marker for identifying high-risk MIRI patients, especially those with coronary artery no-reflow (CNR), who might benefit from targeted therapeutic interventions. Furthermore, Peripheral blood S100A9 in AMI represents a new therapeutic target for preventing MIRI.
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