ArticleMolecular biology reports2025
Upregulation and diagnostic potential of Interleukin-36 cytokine isoforms in dilated cardiomyopathy: evidence from human and murine models.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.Immunogenetics · 2026Article
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Authors and funding
7 authors.
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Abstract
backgroundCardiovascular disease (CVD) is caused by chronic inflammation, however it is yet unknown how interleukin-36 cytokines contribute to coronary artery disease (CAD) and dilated cardiomyopathy (DCM), including how different isoforms affect myocardial remodeling and their possible therapeutic applications.
methodsUsing a publicly available dataset (GSE97320), we conducted transcriptome analysis to investigate IL-36 expression patterns and associated pathways. To find immunological networks and signaling interactors, functional enrichment and protein-protein interaction studies were performed. RT-qPCR was used to evaluate a validation cohort of 300 patients, and results were further validated in a DCM rat model. The diagnostic performance of interleukin-36 isoforms was assessed using Receiver Operating Characteristic (ROC) curve analysis.
resultsThere was a consistent upregulation of interleukin-36 in both DCM and CAD, with IL36G exhibiting the most marked increase (4.9-fold in DCM; p < 0.001). Compared to CAD, expression levels in DCM were noticeably greater. ROC analysis showed good diagnostic accuracy, especially for DCM's IL36A (AUC = 0.98). Interleukin-36 isoform overexpression was verified at the cardiac tissue level in the mouse DCM model. The IL-36R-NF-κB axis is the primary mechanism by which intwerleukin-36 signaling is involved in pro-fibrotic and inflammatory responses, according to pathway and interaction analyses.
conclusionThis study is the first to characterize IL-36 isoforms expression across human and animal models of DCM. Our research provides new insights into the inflammatory landscape of non-ischemic DCM by identifying IL36G as a putative isoform-specific biomarker in myocardial inflammation and remodeling.
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