Abstract
Kawasaki disease (KD) is an acute systemic immune‑mediated vasculitis that can lead to coronary artery lesions. Its etiology remains unclear and may involve immune responses, inflammatory reactions, and vascular endothelial injury mediated by multiple signaling pathways. In recent years, the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway has attracted widespread attention for its pivotal role in infection, autoimmune diseases, and inflammatory diseases. By activating type I interferons and pro-inflammatory mediators, this pathway participates in the inflammatory cascade. This review summarizes the mechanistic roles of the cGAS-STING pathway in KD and the prospects for clinical application, providing a new perspective for basic research and clinical intervention.