VEGF在糖尿病视网膜病变破坏血-视网膜屏障机制中的研究新进展OACSTPCD
Research progress of vascular endothelial growth factor in the mechanism of blood-retinal barrier damage by diabetic retinopathy
糖尿病视网膜病变(DR)是成年人视力下降甚至失明的常见原因之一,由多种发病机制共同作用,其机制虽尚未完全阐明,但血-视网膜屏障破坏是DR的关键过程.血管内皮生长因子(VEGF)作为高度内皮特异的促血管内皮生长因子,是视网膜病理性新生血管形成、破坏血-视网膜屏障的关键因子,因此全面地了解VEGF促进DR血-视网膜屏障破坏的病因病机,成为深入探索DR发病机制的关键.文章围绕DR探讨了 VEGF与视网膜血管内皮细胞间的通透性、血管炎性反应、细胞凋亡反应、氧化应激、线粒体损伤以及内质网应激之间的相关机制,以期为VEGF在DR破坏血-视网膜屏障机制研究提供参考.
Diabetic retinopathy(DR)is one of the common causes of visual impairment and blindness in adults,which is caused by various pathogenesis.Although the mechanism of DR has not been elucidated yet,the destruction of blood-retinal barrier is a key process.As a highly endothelial-specific factor in promoting the growth of vascular endothelial cell,vascular endothelial growth factor(VEGF)plays a crucial role in the formation of pathological retinal neovascularization and the destruction of blood-retinal barrier.Therefore,a comprehensive understanding of the etiology and pathogenesis of blood-retinal barrier damage promoted by VEGF is critical for exploring the pathogenesis of DR.In this study,the underlying relationship between VEGF and the mechanism of blood-retinal barrier damage,including retinal vascular endothelial cell permeability,vascular inflammatory response,apoptosis,oxidative stress,mitochondrial damage and endoplasmic reticulum stress,with a view to providing a reference for the study in VEGF in the pathogenesis of blood-retinal barrier damage in DR.
王苏涵;张乐颖;秦婷婷;王娇娇;宋宗明
(450003)中国河南省郑州市,河南大学人民医院河南省人民医院河南省立眼科医院(453003)中国河南省新乡市,新乡医学院
糖尿病视网膜病变血-视网膜屏障血管内皮生长因子(VEGF)
diabetic retinopathyblood-retinal barriervascular endothelial growth factor(VEGF)
《国际眼科杂志》 2024 (008)
1260-1265 / 6
河南省科技攻关联合共建项目(No.LHGJ20190817);中原科技领军人才项目(No.224200510013);河南省立眼科医院基础研究专项(No.20JCZD001) Joint Project of Medical Science and Technology of Henan Province(No.LHGJ20190817);Central Plains Science and Technology Leading Talents(No.224200510013);Basic Research Project of Henan Eye Hospital(No.20JCZD001)
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