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后发性白内障即后囊膜混浊(PCO),是白内障超声乳化摘出联合人工晶状体植入术后常见的并发症.白内障术后残留的晶状体上皮细胞(LECs)向后囊膜表面移行、增生及上皮-间质转化(EMT)等细胞生物学行为的改变可引起LECs纤维化、PCO及囊袋皱缩.转化生长因子β2(TGF-β2)是目前已知的参与诱导LECs的EMT及组织病理性纤维化关键的细胞因子,它可通过Smad经典通路参与诱导LECs的EMT过程.除此之外,PI3 K/AKT/mTOR信号通路也参与了TGF-β2诱导的EMT过程.RNA干扰(RNAi)技术作为基因调控手段之一,在通过干扰信号通路而抑制LECs的纤维化及增生、迁移等生物学行为中有一定的应用前景.本文就RNAi技术通过干扰PI3 K/AKT/mTOR信号通路和TGF-β2/Smad信号通路对LECs的生物学行为的影响,及其在PCO防治中的作用进行综述.“,”Posterior capsule opacification (PCO) is a common complication after cataract phacoemulsification with intraocular lens (IOL) implantation.The mechanism of lens epithelial cells (LECs) fibrosis,PCO and capsular wrinkle is mainly related with residual LECs migration,proliferation and epithelialmesenchymal transition (EMT) after cataract surgery.Transforming growth factor β2 (TGF-β2) has been proposed as the most important factor driving the EMT and pathologic fibrosis of LECs,TGF-β2 induces LECs EMT by the Smad signaling pathway.Besides,PI3K/AKT/mTOR signaling pathway was studied to participate in TGF-β2 induced EMT.As one of the gene regulation methods,RNA interference (RNAi) technology shows an important application prospect in inhibiting LECs fibrosis and proliferation by interfering signaling pathway.This review highlights RNAi effects on LECs biological behavior by interfering PI3K/AKT/mTOR and TGF-β2/Smad signaling pathways.