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后囊膜混浊(PCO)是白内障囊外手术联合人工晶状体植入术后常见的并发症。白内障术后房水内生长因子含量升高，诱导晶状体上皮细胞(LECs)过度增生、迁移、纤维化导致后囊膜混浊而引起视力下降。PI3K/AKT/mTOR信号通路是调控细胞周期、增生、参与核糖体和蛋白质合成的重要通路，该通路在PCO的发生和发展过程中存在重要的作用。而哺乳动物雷帕霉素靶蛋白(mTOR)是调控PI3K/AKT信号通路蛋白表达的关键位点，应用mTOR抑制剂干预通路信号传递，影响LECs的生物学功能，有望为防治PCO提供新思路。就mTOR信号通路及mTOR抑制剂在PCO发生和发展中的作用研究进展进行阐述。“,”Posterior capsule opacification (PCO) is the most common complication of extracapsular cataract extraction and intraocular lens implantation in the long-term.After cataract surgery, the content of growth factor in aqueous humor increased, which induced excessive hyperplasia, migration and fibrosis of lens epithelial cells (LECs), resulting in posterior capsular opacity and decreased vision.PI3K/AKT/MTOR signaling pathway is an important pathway regulating cell growth, cell cycle, protein and ribosome synthesis, which plays a crucial role in the occurrence and development of PCO.The mammalian target of rapamycin (mTOR) is a key site for regulating the protein expression in the downstream of PI3K/AKT signaling pathway.The application of mTOR inhibitor to interfere with the signaling pathway and affect the biological function of LECs is expected to provide a new idea for the prevention and treatment of PCO.This paper described the research progress of the role of mTOR signaling pathway and mTOR inhibitors in the occurrence and development of PCO.