Han Xiang-Yu, Qi Hui-Ru
Renal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Beijing, China.
Capital Institute of Pediatrics, Peking University Teaching Hospital, Beijing, China.
Front Immunol. 2025 Apr 16;16:1566985. doi: 10.3389/fimmu.2025.1566985. eCollection 2025.
Kawasaki disease (KD) is a relatively common autoimmune disease of childhood, characterized by systemic vasculitis and involvement of the cardiovascular system, particularly the coronary artery. Progressive inflammatory cascades and vascular injury are regarded as two major processes underlying KD. Although it is regarded as a self-limiting disease, some children exhibit resistance to intravenous immunoglobulin (IVIG) treatment, which can lead to the development of life-threatening coronary artery aneurysms that persist into adulthood. Pyroptosis, a special inflammatory cell death pattern, results in the intense release of inflammatory mediators and injuries of tissues such as endothelial cell damage. Evidence from studies and animal models suggests that pyroptosis and associated inflammatory cascades may play a significant role in KD. Here, we highlight the latest insights into pyroptosis in KD and explore the potential therapeutic interventions that target pyroptosis.
川崎病（KD）是儿童期一种相对常见的自身免疫性疾病，其特征为全身性血管炎以及心血管系统受累，尤其是冠状动脉。进行性炎症级联反应和血管损伤被认为是川崎病的两个主要潜在病理过程。尽管川崎病被视为一种自限性疾病，但一些儿童对静脉注射免疫球蛋白（IVIG）治疗有抵抗性，这可能导致威胁生命的冠状动脉瘤的形成，并持续至成年期。细胞焦亡是一种特殊的炎症性细胞死亡模式，会导致炎症介质的大量释放以及诸如内皮细胞损伤等组织损伤。来自研究和动物模型的证据表明，细胞焦亡及相关炎症级联反应可能在川崎病中起重要作用。在此，我们重点介绍川崎病中细胞焦亡的最新见解，并探索针对细胞焦亡的潜在治疗干预措施。
