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Demonstrates that interleukin-1 inhibition ameliorates cardiac dysfunction and arrhythmias in murine Kawasaki disease, highlighting therapeutic targets for systemic vasculitis.
Kawasaki disease (KD) is an acute febrile illness and systemic vasculitis often associated with cardiac sequelae, including arrhythmias. Abundant evidence indicates a central role for IL (interleukin)-1 and TNFα (tumor necrosis factor-alpha) signaling in the formation of arterial lesions in KD. We aimed to investigate the mechanisms underlying the development of electrophysiological abnormalities in a murine model of KD vasculitis.
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Mesquita et al. (2024) studied this question.
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