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Role of adiponectin in fundus neovascularization disease / 中华实验眼科杂志
Article em Zh | WPRIM | ID: wpr-1022840
Biblioteca responsável: WPRO
ABSTRACT
Fundus neovascularization disease is a series of clinicopathological changes caused by pathological vascular growth of choroid and retina.It is a kind of fundus disease that seriously affects vision.At present, it is believed that the main cause of the disease is the imbalance between the promoters and inhibitors of angiogenesis.Currently widely used drugs against vascular endothelial growth factor (VEGF) are still ineffective in many patients with fundus neovascularization.Adiponectin (APN) is an endogenous bioactive protein secreted by adipocytes, which has the functions of increasing insulin sensitivity, regulating sugar and lipid metabolism, anti-inflammatory, and inhibiting neovascularization.In recent years, it has been found that APN and its receptors play an important role in fundus neovascularization diseases.Many studies have demonstrated the clinical predictive value of APN gene polymorphism in fundus neovascularization diseases. In vivo and in vitro models have verified the important proportion of APN in the pathological mechanism of chronic inflammation and neovascularization.The mechanism may be that APN inhibits VEGF-stimulated endothelial cell migration, and maintains normal vascular endothelial cell function .At this point we do not know whether APN is pro or anti angiogenic molecule in eye.Understanding the role of APN and its receptors in fundus neovascularization diseases is expected to provide potential therapeutic targets and new ideas for the prevention and treatment of fundus neovascularization diseases.This article reviews the role of APN and its receptor in fundus retinal neovascularization disease.
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Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Experimental Ophthalmology Ano de publicação: 2024 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Experimental Ophthalmology Ano de publicação: 2024 Tipo de documento: Article