Roy Sayon, Kim Dongjoon, Lim Remington
Department of Medicine and Ophthalmology, Boston University School of Medicine, Boston, MA, United States.
Department of Medicine and Ophthalmology, Boston University School of Medicine, Boston, MA, United States.
Vision Res. 2017 Oct;139:115-122. doi: 10.1016/j.visres.2017.04.014. Epub 2017 Jun 28.
In diabetic retinopathy, high glucose (HG)-mediated breakdown in cell-cell communication promotes disruption of retinal homeostasis. Several studies indicate that HG condition alters expression of connexin genes and subsequent gap junction intercellular communication (GJIC) in retinal vascular cells and non-vascular cells. A serious consequence of disrupted cell-cell communication is apoptosis and breakdown of the blood-retinal barrier (BRB). More recently, studies suggest adverse effects from HG on retinal Müller cells. This article focuses on HG-mediated changes in connexin expression and GJIC and their subsequent effects on the breakdown of retinal homeostasis, cell death, compromised vascular permeability, and interactions between endothelial cells, pericytes and retinal Müller cells in the pathogenesis of diabetic retinopathy. Additionally, options for rectifying disrupted homeostasis under HG condition associated with diabetic retinopathy are reviewed.
在糖尿病视网膜病变中，高糖（HG）介导的细胞间通讯破坏会促进视网膜内环境稳态的紊乱。多项研究表明，HG状态会改变视网膜血管细胞和非血管细胞中连接蛋白基因的表达以及随后的间隙连接细胞间通讯（GJIC）。细胞间通讯破坏的一个严重后果是细胞凋亡和血视网膜屏障（BRB）的破坏。最近，研究表明HG对视网膜穆勒细胞有不良影响。本文重点关注HG介导的连接蛋白表达和GJIC变化及其随后对糖尿病视网膜病变发病机制中视网膜内环境稳态破坏、细胞死亡、血管通透性受损以及内皮细胞、周细胞和视网膜穆勒细胞之间相互作用的影响。此外，还综述了纠正与糖尿病视网膜病变相关的HG条件下内环境稳态破坏的方法。
