Endothelial dysfunction is central to the pathogenesis of Kawasaki disease and its cardiovascular complications, highlighting potential therapeutic targets to mitigate vascular damage.
This review highlights the role of endothelial dysfunction in Kawasaki disease pathogenesis and the need to translate preclinical findings into targeted therapies to prevent cardiovascular complications.
The endothelium plays a key role in regulating vascular homeostasis by responding to a large spectrum of chemical and physical stimuli. Vasculitis is a group of inflammatory conditions affecting the vascular bed, and it is known that they are strongly linked to endothelial dysfunction (ED). Kawasaki disease (KD) is one childhood systemic vasculitis, and it represents the leading cause of acquired cardiac disease in children due to coronary damage and subsequent cardiovascular (CV) morbidity and mortality. We aimed to focus on the actual knowledge of ED in the pathogenesis of KD and its practical implications on therapeutical strategies to limit cardiovascular complications. Understanding ED in KD provides insight into the underlying mechanisms and identifies potential therapeutic targets to mitigate vascular damage, ultimately improving cardiovascular outcomes in both the acute and chronic stages of the disease. However, research gaps remain, particularly in translating findings from animal models into clinical applications for cardiovascular lesions and related morbidity in KD patients.
Paolini et al. (Thu,) conducted a review in Kawasaki disease. Therapeutic strategies targeting endothelial dysfunction was evaluated. Endothelial dysfunction is central to the pathogenesis of Kawasaki disease and its cardiovascular complications, highlighting potential therapeutic targets to mitigate vascular damage.