Tissue remodeling in vascular wall in Kawasaki disease-related vasculitis model mice

Abstract

Kawasaki disease is the most common acute systemic vasculitis of unknown etiology in children [1] and can cause inflammation of the coronary arteries leading to aneurysms. Tenascin-C, an extracellular matrix protein, and c-Jun N-terminal kinase (JNK), an intracellular signaling protein, are known to be associated with inflammation and tissue remodeling [2, 3]. The purpose of this study was to demonstrate tenascin-C and JNK might be involved in tissue remodeling in a Candida albicans-induced murine model of aneurysm.