ArticleFrontiers in cardiovascular medicine2025
Alterations in bile acid metabolites associated with pathogenicity and IVIG resistance in Kawasaki disease.
Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Metabolic reprogramming rewires aberrant immune responses to drive endothelial dysfunction in Kawasaki disease: a narrative review.Translational pediatrics · 2026Review
- The Autophagy-Inflammation Axis in Kawasaki Disease: Pathogenic Mechanisms and Translational Opportunities.Journal of clinical medicine · 2026Review
- Multiomics approaches in Kawasaki disease: insights into pathogenesis and emerging directions for diagnosis and treatment.Clinical and experimental pediatrics · 2026Article
- Hepatobiliary involvement in Kawasaki disease: from cholestatic hepatitis to the hepatic vascular-biliary unit hypothesis-a state-of-the-art review.Frontiers in immunology · 2026Review
- Lysophosphatidylcholine as a Novel Diagnostic Biomarker in Kawasaki Disease: Based on Immunometabolism-Related Signature.Journal of inflammation research · 2025Article
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Authors and funding
7 authors.
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Abstract
Background: Kawasaki disease (KD) primarily affects children as an acute systemic vasculitis. Numerous studies indicated an elevated risk of cardiovascular disease due to metabolic disturbances. Despite this knowledge, the specific metabolic modes involved in KD remain unclear. Methods: We examined the metabolome of individuals with 108 KD and 52 non-KD controls (KD vs. nKD) by ultraperformance liquid chromatography (UPLC) and tandem mass spectrometry (MS). Results: Differential analysis uncovered the disturbed production of bile acids and lipids in KD. Furthermore, we investigated the impact of treatment, intravenous immunoglobulin (IVIG) resistance, and coronary artery (CA) occurrence on the metabolome. Our findings suggested that IVIG treatment alters the lipid and amino acid metabolism of KD patients. By orthogonal projections to latent structures discriminant analysis (OPLS-DA), there was no significant difference between the coronary injury groups and non-coronary injury groups, and IVIG resistance didn't appear to cause the metabolic change in KD patients. Conclusions: Patients with KD exhibit metabolic abnormalities, particularly in bile acids and lipids. IVIG interventions may partially ameliorate these lipid abnormalities.
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