期刊文献+

整合素连接激酶在白内障发病过程中的作用 被引量:4

The role of integrin-linked kinase in the pathogenesis of cataract
下载PDF
导出
摘要 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。 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.
作者 俞晶晶 郑志
出处 《中华实验眼科杂志》 CAS CSCD 北大核心 2017年第3期282-285,共4页 Chinese Journal Of Experimental Ophthalmology
关键词 整合素连接激酶 整合素 水通道蛋白 白内障 发病机制 Integrin-linked kinase Integrin Aquaporin Cataract Pathogenesis
  • 相关文献

参考文献3

二级参考文献30

  • 1韩小霞,惠延年,宋虎平,王海涛,张晓光,刘百军.高浓度葡萄糖对培养的人视网膜色素上皮细胞细胞表面黏附分子-1的影响[J].国际眼科杂志,2006,6(2):317-320. 被引量:11
  • 2Grashoff C, Thievessen I, Lorenz K, et al. Integrin-linked kinase: integrin' s mysterious parter [ J ]. Curr Opin Cell Biol, 2004,16 ( 5 ) : 565 - 571 被引量:1
  • 3Ebihara Y, Kato S, Oshika T, et al. Posterior capsule opacification after cataract surgery in patients with diabetes mellitus[ J]. J Cataract Refract Surg, 2006,32 ( 7 ) : 1184 - 1187 被引量:1
  • 4Walker J, Menko AS. Integrins in lens development and disease [ J ]. Exp Eye Res,2008,11:1 - 10 被引量:1
  • 5Han SY, Kang YS, Jee YH, et al. High glucose and angiotensin Ⅱ increase β1 integrin and integrin-linked kinase synthesis in cultured mouse podocytes [ J ]. Cell Tissue Res, 2006,323 ( 2 ) : 321 - 332 被引量:1
  • 6Ohnishi M, Hasegawa G, Yamasaki M, et al. Integrin-linked kinase acts as a pro-survival factor against high glucose-associated osmotic stress in human mesangial cells [ J ]. Nephrol Dial Transplant, 2006, 21 ( 7 ) : 1786 - 1793 被引量:1
  • 7Liu XC,Liu BC, Zhang XL, et al. Role of ERK1/2 and PI3-K in the regulation of CTGF-induced ILK expression in HK-2 cells[ J]. Clin Chim Acta, 2007,382 ( 1 - 2) : 89 - 94 被引量:1
  • 8Bras ID,Colitz CM, Kusewitt DF, et al. Evaluation of advanced glycation end-products in diabetic and inherited canine cataracts [ J ]. Graefe' s Arch Clin Exp Ophthalmol,2007,245 (2) : 249 - 257 被引量:1
  • 9Harper JW, Elledge SJ, Keyomarsi K, et al. Inhibition of cyclin- dependent-kinases by p21 [ J ]. Mol Biol Cell, 1995,6 (4) : 387 - 400 被引量:1
  • 10Tkachoy SI, Lautenschlager C, Ehrich D, et al. Changes in the lens epithelium with respect to cataractogenesis-Light microscopic and Scheimpflug densitometric and the cataractous and the clear lens of diabetics and non-diabetics [ J ]. Graefe' s Arch Clin Exp Ophthalmol, 2006,244(5 ) : 596 - 602 被引量:1

共引文献14

同被引文献32

引证文献4

二级引证文献18

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部