[关键词]
[摘要]
Fuchs角膜内皮营养不良(FECD)是以角膜内皮进行性损害，逐渐发展为角膜内皮失代偿为特征的一种营养不良性疾病，目前的标准疗法即角膜移植手术存在种种限制。最近的研究发现，Rho相关激酶抑制剂可通过调节细胞周期蛋白D和p27信号传导通路促进细胞增殖，激活Rac1蛋白驱动肌动蛋白相关蛋白复合物(ARPC2)增加细胞黏附，调节膜出泡、核崩解和凋亡小体的形成抑制角膜内皮细胞的凋亡，有望治疗FECD。文章主要对Rho相关激酶抑制剂治疗FECD的药理作用、基础研究、临床试验以及不良反应等相关进展进行综述，希望能尽早开发出疗效稳定且副作用少的化合物，为治疗FECD提供新方案。
[Key word]
[Abstract]
Fuchs endothelial corneal dystrophy(FECD)is a progressive dystrophic disease characterized by gradual damage to the corneal endothelium, ultimately leading to endothelial decompensation. The current standard treatment, corneal transplantation, has several limitations. Recent studies have shown that Rho-associated kinase(ROCK)inhibitors can promote cell proliferation by modulating the cyclin D and p27 signaling pathways. Additionally, ROCK inhibitors activate Rac1, which drives the actin-related protein complex(ARPC2)to enhance cell adhesion, and regulate processes such as membrane blebbing, nuclear disintegration, and apoptotic body formation, thereby inhibiting the apoptosis of corneal endothelial cells. These findings suggest that ROCK inhibitors may be a promising therapeutic approach for FECD. This review provides an overview of the pharmacological effects, basic research, clinical trials, and potential adverse reactions associated with ROCK inhibitors in the treatment of FECD, with the aim of developing compounds with stable efficacy and minimal side effects for the treatment of FECD in the near future.
[中图分类号]
[基金项目]
国家自然科学基金项目(No.U20A20363)
