糖尿病视网膜病变(Diabetic retinopathy, DR)是成人致盲的主要原因之一,目前认为VEGF在DR的进展中占据重要地位,却缺乏对其上下游环节的研究,而血管内皮细胞钙粘蛋白(Vascular endothelial cell cadherin, VE-cadherin)作为VEGF介导的...糖尿病视网膜病变(Diabetic retinopathy, DR)是成人致盲的主要原因之一,目前认为VEGF在DR的进展中占据重要地位,却缺乏对其上下游环节的研究,而血管内皮细胞钙粘蛋白(Vascular endothelial cell cadherin, VE-cadherin)作为VEGF介导的信号通路的下游环节与视网膜血管通透性改变、视网膜屏障破坏及新生血管形成密切相关。本文分析了VE-cadherin在维持DR血管结构和功能稳定、血管形成、炎症反应中起到的重要作用,发现通过调节其表达和磷酸化状态,可能有助于防止血管渗漏和新生血管形成,因此我们推测VE-cadherin可能是治疗DR的潜在靶点。Diabetic retinopathy (DR) is the major cause of severe vision loss in adults. Currently, VEGF is recognized to play a pivotal role in the progression of DR, yet there is a lack of research on its upstream and downstream mechanisms. Vascular endothelial cell cadherin (VE-cadherin), as a downstream component of VEGF-mediated signaling pathways, is closely associated with alterations in retinal vascular permeability, disruption of the retinal barrier, and neovascularization. This paper analyzes the crucial role of VE-cadherin in maintaining the stability of vascular structure and function, angiogenesis and inflammatory responses in DR. It is also found that by modulating its expression and phosphorylation status, it may help prevent vascular leakage and neovascularization. Therefore, we hypothesize that VE-cadherin could be a potential therapeutic target for the treatment of DR.展开更多
文摘糖尿病视网膜病变(Diabetic retinopathy, DR)是成人致盲的主要原因之一,目前认为VEGF在DR的进展中占据重要地位,却缺乏对其上下游环节的研究,而血管内皮细胞钙粘蛋白(Vascular endothelial cell cadherin, VE-cadherin)作为VEGF介导的信号通路的下游环节与视网膜血管通透性改变、视网膜屏障破坏及新生血管形成密切相关。本文分析了VE-cadherin在维持DR血管结构和功能稳定、血管形成、炎症反应中起到的重要作用,发现通过调节其表达和磷酸化状态,可能有助于防止血管渗漏和新生血管形成,因此我们推测VE-cadherin可能是治疗DR的潜在靶点。Diabetic retinopathy (DR) is the major cause of severe vision loss in adults. Currently, VEGF is recognized to play a pivotal role in the progression of DR, yet there is a lack of research on its upstream and downstream mechanisms. Vascular endothelial cell cadherin (VE-cadherin), as a downstream component of VEGF-mediated signaling pathways, is closely associated with alterations in retinal vascular permeability, disruption of the retinal barrier, and neovascularization. This paper analyzes the crucial role of VE-cadherin in maintaining the stability of vascular structure and function, angiogenesis and inflammatory responses in DR. It is also found that by modulating its expression and phosphorylation status, it may help prevent vascular leakage and neovascularization. Therefore, we hypothesize that VE-cadherin could be a potential therapeutic target for the treatment of DR.
