ArticleJournal of cellular and molecular medicine2025
Potential Inflammatory Mediators in Pericardial Fluids of Patients With Coronary Artery Diseases and Their Association With Plasma Biomarkers.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to determine the gene expression and protein levels of interleukin-33 (IL-33), fetuin A and cytokeratin 18 (CK-18) in the pericardial fluid (PF) and plasma of patients with coronary artery disease (CAD) undergoing coronary artery bypass grafting (CABG). The CAD patients (mean age: 73.4 years) were enrolled. The IL-33, fetuin A, and CK-18 protein levels in pericardial fluid (PF) and plasma of patients with CAD were measured by ELISA, while IL-33 and Fetuin A gene expressions were analysed via quantitative reverse transcription-PCR (qRT-PCR). The IL-33 protein level in PF was significantly higher than plasma (PF: 57.09 ng/L; Plasma: 50.15 ng/L; p < 0.05). Similarly, the fetuin A protein levels were significantly elevated in PF compared to plasma (PF: 1060.53 mg/L; Plasma: 725.85 mg/L; p < 0.05). However, gene expression levels (ΔCt values) for IL-33 and fetuin A were significantly higher in plasma than in PF (p < 0.05). The CK-18 protein levels were comparable between plasma and PF (p > 0.05). Strong positive correlations were observed between CK-18 and IL-33 (r = 0.127, p < 0.001) and between CK-18 and fetuin A (r = 0.096, p < 0.001) in PF. The IL-33, fetuin A, and CK-18 levels in PF are predicted to have the potential to be used as a source of biomarkers for CAD. Although the collection of PF samples requires an invasive procedure, the proximity of PF to the heart tissue makes it a valuable source for understanding cardiac pathophysiology. These findings highlight the potential diagnostic and therapeutic utility of PF biomarkers in patients with CAD.
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