郭 佳,白玉芳,李舒敏,马君慧,宋 颎

胎膜早破（PROM）是围产期常见的并发症，可导致宫内感染、新生儿呼吸暂停、早产甚至胎儿死亡等不良后果。已知细胞外基质在整个妊娠期间有助于胎膜的结构完整性，细胞外基质的过度降解可由胎膜组织中核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）的异常活化引起，该机制的核心在于炎症因子驱动的基质金属蛋白酶（MMPs）上调表达，以及消皮素D（Gasdermin D）介导的细胞焦亡共同破坏胎膜组织架构，本综述重点探讨NLRP3与PROM之间的关联性，以增进对PROM病理机制及临床干预的认知水平。

胎膜早破；核苷酸结合寡聚化结构域样受体蛋白3；炎症小体；基质金属蛋白酶；细胞焦亡

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