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冠状动脉损害(CAL)是川崎病(KD)的主要并发症,现已成为儿童最常见的后天性心脏病之一。近年来研究表明,川崎病冠状动脉损害与血管壁细胞外基质(ECM)降解有关,而血管壁细胞外基质降解与基质金属蛋白酶(matrix metalloproteinases,MMPs)激活和(或)与其组织抑制剂(tissue inhibitor of matrix metalloprotein-ases,TIMPs)的平衡被破坏有关。因此,基质金属蛋白酶(MMPs)及其抑制剂(TIMPs)在川崎病冠脉损害的发生发展中起着重要作用,应用TIMPs对MMPs水平进行调控是KD治疗及预防冠脉并发症的一个新方向。
Coronary artery lesions (CALs) are a major complication of Kawasaki disease (KD) and have now become one of the most common forms of acquired heart disease in children. In recent years, studies have shown that coronary artery lesions in Kawasaki disease are associated with the degradation of extracellular matrix (ECM) in the vascular wall, whereas the degradation of extracellular matrix in the vascular wall is associated with the activation of matrix metalloproteinases (MMPs) and / inhibitor of matrix metalloprotein-ases, TIMPs) is destroyed. Therefore, matrix metalloproteinases (MMPs) and its inhibitors (TIMPs) play an important role in the development of coronary artery lesions in Kawasaki disease. The regulation of MMPs using TIMPs is a new direction of KD treatment and prevention of coronary complications .