已发表论文

溶血磷脂酰胆碱作为川崎病的新型诊断生物标志物:基于免疫代谢相关特征

 

Authors Ma X, Zheng Y, Feng C, Zhang M, Wang H, Li X

Received 22 October 2025

Accepted for publication 19 December 2025

Published 31 December 2025 Volume 2025:18 Pages 18343—18355

DOI https://doi.org/10.2147/JIR.S567612

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Qing Lin

Xiaomei Ma,1,* Yang Zheng,2,* Chenhui Feng,1 Mingming Zhang,3 Hongmao Wang,3 Xiaohui Li1– 3 

1Capital Institute of Pediatrics-Peking University Teaching Hospital, Beijing, People’s Republic of China; 2Capital Institute of Pediatrics, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, People’s Republic of China; 3Department of Cardiovascular Medicine, Capital Center for Children’ s Health, Capital Medical University, Beijing, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Xiaohui Li, Capital Institute of Pediatrics-Peking University Teaching Hospital, No. 2, Yabao Road, Chaoyang District, Beijing, 100020, People’s Republic of China, Email lxhmaggie@pumc.edu.cn

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.

Keywords: Kawasaki disease, metabolomics, targeted lipidomics, single-cell RNA sequencing, lysophosphatidylcholine