Multiomics approaches in Kawasaki disease: insights into pathogenesis and emerging directions for diagnosis and treatment

Abstract

Kawasaki disease (KD) is an acute febrile vasculitis and the leading cause of acquired heart disease in children. Despite decades of research, the etiology remains un known and key mechanisms linking systemic inflamma tion to coronary artery lesions are incompletely defined. High throughput technologies-including genomics, transcriptomics, proteomics, metabolomics, epigenomics, and immunomics-have enabled systems level profiling of KD and highlighted reproducible inflammatory and vascular pathways. Multiomics integration increasingly supports convergent mechanistic axes, particularly inter leukin (IL1/IL6-neutrophil programs, Fc gamma receptor sig naling related to intravenous immunoglobulin (IVIG) pharmacodynamics, Ca2+/nuclear factor of activated T cells dependent T cell activation, and endothelial/extra cellular matrix remodeling associated with coronary outcomes. While these findings provide a robust frame work for biomarker discovery and therapeutic hypothesis generation, most signatures remain investigational and require prospective validation, standardized sampling (pre/postIVIG), and clinically scalable assays before rou tine implementation. This review summarizes current multiomics applications in KD, prioritizes the most con sistently supported pathways, and outlines a pragmatic roadmap toward clinically useful risk stratification, dis ease monitoring, and outcome prediction.