ArticleJournal of inflammation research2025
MFG-E8 in Kawasaki Disease: Role in Endothelial Injury and Diagnostic Potential.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
- FOS regulation of T-cell activation and the mechanism of inflammatory injury of coronary endothelium in Kawasaki disease.Translational pediatrics · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Kawasaki disease (KD) is a systemic vasculitis predominantly affecting children under five years old, with coronary artery lesions (CALs) being a severe complication. Despite the effectiveness of intravenous immunoglobulin (IVIG) therapy, a subset of patients remains unresponsive, necessitating alternative strategies. Milk Fat Globule Epidermal Growth Factor 8 (MFG-E8) is a secreted glycoprotein that functions as a bridge between damaged cells and phagocytes, conferring the ability to regulate immunity and inflammation. This study aimed to investigate the potential role of MFG-E8 in KD pathogenesis. Methods: Serum levels of MFG-E8 were measured via ELISA. CAWS was utilized to induce a murine model of coronary vasculitis, with MFG-E8 being administered intraperitoneally for treatment. Histological evaluation was conducted using H&E and IHC staining. Serum-stimulated THP-1 cells were co-cultured with endothelial cells to establish an inflammatory environment in vitro, with exogenous supplementation of MFG-E8. Pyroptosis-related markers were assessed by Western blot or immunofluorescence staining. Oxidative stress-related indicators were measured using commercially available assay kits. Results: Serum MFG-E8 levels were significantly lower in KD patients, especially those with CALs, compared to febrile and healthy controls. ROC analysis showed that combining MFG-E8 with Fbg and TT improved the ability to distinguish KD from other febrile illnesses. Further analyses displayed negative correlations between MFG-E8 and parameters pointing to inflammation. In the murine model of vasculitis, MFG-E8 supplementation alleviated coronary artery inflammation, reduced endothelial cell pyroptosis, and mitigated oxidative stress. Similar results were presented in vitro experiments using KD serum-treated endothelial cells. Conclusion: MFG-E8 represents a potential biomarker for the diagnosis of KD and exhibits protective effects against endothelial cell injury during the acute phase.
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