ArticleJournal of inflammation research2025
Lysophosphatidylcholine as a Novel Diagnostic Biomarker in Kawasaki Disease: Based on Immunometabolism-Related Signature.
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 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Natural flavonoid isoorientin and its anticancer mechanisms: a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2026Pooled it
- Cancer Gene Therapy Utilizing NF-κB-regulated Expression of a miRNA Targeting RelA.Applied biochemistry and biotechnology · 2026Article
- Gatekeepers of immunity: mechanisms and regulation of immune checkpoints and their role in immune-privileged sites.Molecular biology reports · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Kawasaki disease (KD) is a systemic vasculitis of unknown etiology. Delayed diagnosis and treatment elevate the risk of coronary artery complications. This study aims to investigate metabolic disorders associated with its potential pathophysiology and to explore novel diagnostic biomarkers. Patients and Methods: Untargeted metabolomics was used to identify significantly dysregulated metabolic pathways in patients with KD. Targeted lipidomic analysis was performed to detect differentially expressed lipid metabolites. Candidate plasma biomarkers were quantified using ELISA. Single-cell RNA sequencing was used to analyze the expression of lipid metabolism-related genes and cellular heterogeneity. Results: Sphingolipid metabolism was confirmed to be dysregulated in patients with KD. Twelve differentially expressed lipid species were identified: 20:5-carnitine, sphingomyelin 32:2;O2, ceramide d16:0/24:0, glucosylceramide d18:1/26:0, lysophosphatidylcholine (LPC) O-16:0, LPC 17:0, LPC 18:0, and phosphatidylcholine (PC) 32:2, PC 36:3, PC 40:3, PC 40:4, and PC 40:7. ELISA validation confirmed the lipidomics-identified alterations in LPC. As a diagnostic biomarker, LPC achieved an area under the curve (AUC) of 0.768, with 64.7% sensitivity and 88.2% specificity. Single-cell RNA sequencing data revealed a marked accumulation of monocytes in KD, along with upregulated expression of lipid metabolism-associated genes. Notably, the expression levels of inflammatory genes were altered along with those of LPC degradation-related genes in monocytes from patients with KD. Conclusion: This study demonstrated significant dysregulation of lipid metabolism in KD, potentially driven by inflammatory responses in monocytes. LPC has emerged as a potential biomarker of KD and provides new insights into its early diagnosis.
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