Role of Programmed Cell Death in the Pathogenesis of Kawasaki Disease: Mechanisms and Therapeutic Implications

Programmed cell death (PCD) is a genetically regulated, orderly cell death process essential for tissue homeostasis. Contemporary PCD comprises a broad spectrum, including apoptosis, pyroptosis, ferroptosis, necroptosis, autophagy-dependent cell death, NETosis, parthanatos, and entotic cell death. Kawasaki disease (KD) is an acute pediatric systemic vasculitis and a leading cause of acquired childhood heart disease, with coronary artery lesions as the most severe complication. Mounting evidence confirms that PCD is tightly associated with KD-related vascular endothelial injury and inflammatory amplification. Among all PCD subtypes, apoptosis, pyroptosis, and ferroptosis have the most sufficient and direct evidence in KD pathogenesis, mediating vascular wall damage and inflammatory imbalance via distinct molecular pathways. This review focuses on these three well-documented PCD forms (with a brief overview of other PCD subtypes and their potential KD relevance), systematically elaborates their crosstalk with KD pathogenesis, summarizes current research progress, and proposes targeted therapeutic strategies for KD.