ArticleFrontiers in pediatrics2025
Combination of CRP and miRNA signature as a potential diagnostic strategy for Kawasaki disease.
Article in Frontiers in pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Extracellular Vesicles Derived from Resveratrol-Treated BMSCs Promote the Repair of Bone Defects in Osteoporotic Rats.Stem cell reviews and reports · 2026Article
- Multiomics approaches in Kawasaki disease: insights into pathogenesis and emerging directions for diagnosis and treatment.Clinical and experimental pediatrics · 2026Article
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8 authors.
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Abstract
Background: Kawasaki disease is the leading cause of acquired heart disease in children, yet timely diagnosis remains difficult due to overlapping symptoms with other febrile illnesses. Methods: In a retrospective case-control study of 38 children with Kawasaki disease and 44 febrile controls, we measured hematological parameters and C-reactive protein (CRP) using standardized analyzers and profiled seven serum microRNAs by qRT-PCR. Biomarkers showing significant differences were used to build logistic regression models with a 70/30 train-test split, and diagnostic accuracy was assessed by receiver operating characteristic analysis. Functional enrichment of miRNA targets was explored using network analysis. Results: CRP and three microRNAs (miR-223-3p, miR-19a-3p, miR-18a-5p) were significantly elevated in Kawasaki disease. Individually, these markers achieved strong discrimination (AUC: 0.846-0.986), while their combination yielded an AUC of 0.990, sensitivity 1.000, and specificity 0.923. The three microRNAs were positively correlated and enriched for pathways including p53 signaling and cell cycle regulation, with KCNQ1OT1 identified as a shared lncRNA interactor. Conclusion: Integrating CRP with a concise serum miRNA panel demonstrates promising discriminatory potential for Kawasaki disease vs. other febrile illnesses and suggests mechanistic involvement of p53-associated pathways, supporting future validation in larger, independent cohorts.
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