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The role of integrin-linked kinase in the pathogenesis of cataract / 中华实验眼科杂志
Chinese Journal of Experimental Ophthalmology ; (12): 282-285, 2017.
Artigo em Chinês | WPRIM | ID: wpr-638182
ABSTRACT
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.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo de etiologia / Fatores de risco Idioma: Chinês Revista: Chinese Journal of Experimental Ophthalmology Ano de publicação: 2017 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo de etiologia / Fatores de risco Idioma: Chinês Revista: Chinese Journal of Experimental Ophthalmology Ano de publicação: 2017 Tipo de documento: Artigo