整合素连接激酶在白内障发病过程中的作用

整合素是一种在哺乳动物体内广泛表达的细胞表面受体,整合素连接激酶(ILK)是整合素信号通路的关键激酶,其与整合素结合进行细胞与细胞外基质(ECM),甚至细胞与细胞之间的信号传导.目前的研究发现,ILK及其整合素信号通路的活化可以激活磷脂酰肌醇-3-激酶/丝苏氨酸蛋白激酶(PI3K/AKT)和转化生长因子β/Smad蛋白(TGF-β/Smad)介导的细胞增生、黏附和迁移,引起晶状体上皮细胞异常增生和纤维化,还能激活糖原合成酶激酶3β/β-链蛋白(GSK3β/β-catenin)等信号通路,介导水通道蛋白(AQPs)调节水转运过程,最终导致晶状体内囊泡运输受限,渗透压改变,从而引起白内障.白内障是世界主要的致盲眼病之一,其主要由于老化、遗传、代谢异常、外伤、辐射、中毒和局部营养不良等引起的晶状体囊膜损坏,使其渗透性增加,丧失屏障作用,或导致晶状体代谢紊乱,使晶状体蛋白发生变性,形成混浊,但其发病机制尚未完全阐明.ILK可以通过多种信号通路介导人晶状体上皮细胞的移行、黏附、增生和凋亡,因此深入研究ILK在白内障发病中的作用对白内障的预防和治疗有重要意义.本文就近年来ILK在白内障发病中的作用进行综述.

The role of integrin-linked kinase in the pathogenesis of cataract

Integrin is a cell surface receptor that is widely expressed in mammals.Integrin-linked kinase (ILK) is a key kinase of the integrin signaling pathway which combines with integrins to communicate cell and extracellular matrix.Recent studies have shown that ILK can activate phosphatidylinositol-3-kinase/serine protein kinase (PI3K/AKT) and transforming growth factor beta/Smad (TGF-β/Smad) signaling pathways,which can promote cell proliferation,adhesion and migration of lens epithelial cells.It also can activate glycogen synthase kinase 3β/β-catenin (GSK3β/β-catenin) and other signaling pathways mediate aquaporins to regulate the water transport process.Eventually these changes can affect osmotic pressure of lens and lead to the formation of cataract.Cataract is a leading cause of visual impairment worldwide.It is a multi-factorial optic disorder associated with various risk factors such as aging,genetic,metabolic abnormalities,trauma,ultraviolet light exposure,poisoning and malnutrition.But the pathogenesis of cataract is not fully understood.ILK can mediate the migration,adhesion,proliferation and apoptosis of human lens epithelial cells through a variety of signaling pathways.Therefore,it is very important to study the role of ILK in the pathogenesis of cataract in the prevention and treatment of cataract.In this article,we reviewed the role of ILK in the pathogenesis of cataract from recent years.