Liu Yuxuan, Dong Xiaoming, Wu Bin, Cheng Zhigang, Zhang Jinsong, Wang Jing
AIER Cataract Institute Shenyang Liaoning Province 110000 China.
Shenyang Aier Ophthalmology Institute of Precision Medicine Shenyang Liaoning Province 110000 China.
Glob Chall. 2024 Nov 12;8(12):2400181. doi: 10.1002/gch2.202400181. eCollection 2024 Dec.
Phacoemulsification combined with intraocular lens implantation is the primary treatment for cataract. Although this treatment strategy benefits patients with cataracts, posterior capsule opacification (PCO) remains a common complication that impairs vision and affects treatment outcomes. The pathogenesis of PCO is associated with the proliferation, migration, and fibrogenesis activity of residual lens epithelial cells, with epithelial-mesenchymal transition (EMT) serving as a key mechanism underlying the condition. Transforming growth factor-beta 2 (TGF-β2) is a major promotor of EMT, thereby driving PCO development. Most studies have shown that drugs and miRNAs mitigate EMT by inhibiting, clearing, or eliminating LECs. In addition, targeting EMT-related signaling pathways in TGF-β2-stimulated LECs has garnered attention as a research focus. This review highlights potential treatments for PCO and details the mechanisms by which drugs and miRNAs counter EMT.
超声乳化白内障吸除联合人工晶状体植入术是白内障的主要治疗方法。尽管这种治疗策略使白内障患者受益,但后囊膜混浊(PCO)仍然是一种常见的并发症,会损害视力并影响治疗效果。PCO的发病机制与残留晶状体上皮细胞的增殖、迁移和纤维化活动有关,上皮-间质转化(EMT)是该疾病的关键机制。转化生长因子-β2(TGF-β2)是EMT的主要促进因子,从而推动PCO的发展。大多数研究表明,药物和微小RNA通过抑制、清除或消除晶状体上皮细胞来减轻EMT。此外,针对TGF-β2刺激的晶状体上皮细胞中与EMT相关的信号通路已成为研究热点。本综述重点介绍了PCO的潜在治疗方法,并详细阐述了药物和微小RNA对抗EMT的机制。