Kaur C, Foulds W S, Ling E A
Department of Anatomy, Yong Loo Lin School of Medicine, Block MD10, 4 Medical Drive, National University of Singapore, Singapore 117597, Singapore.
Prog Retin Eye Res. 2008 Nov;27(6):622-47. doi: 10.1016/j.preteyeres.2008.09.003. Epub 2008 Oct 4.
The blood-retinal barrier (BRB) plays an important role in the homeostatic regulation of the microenvironment in the retina. It consists of inner and outer components, the inner BRB (iBRB) being formed by the tight junctions between neighbouring retinal capillary endothelial cells and the outer barrier (oBRB) by tight junctions between retinal pigment epithelial cells. Astrocytes, Müller cells and pericytes contribute to the proper functioning of the iBRB. In many clinically important conditions including diabetic retinopathy, ischaemic central retinal vein occlusion, and some respiratory diseases, retinal hypoxia results in a breakdown of the iBRB. Disruption of the iBRB associated with increased vascular permeability, results in vasogenic oedema and tissue damage, with consequent adverse effects upon vision. Factors such as enhanced production of vascular endothelial growth factor (VEGF), NO, oxidative stress and inflammation underlie the increased permeability of the iBRB and inhibition of these factors is beneficial. Experimental studies in our laboratory have shown melatonin to be a protective agent for the iBRB in hypoxic conditions. Although oBRB breakdown can occur in conditions such as accelerated hypertension and the toxaemia of pregnancy, both of which are associated with choroidal ischaemia and in age-related macular degeneration (ARMD), and is a feature of exudative (serous) retinal detachment, our studies have shown that the oBRB remains intact in hypoxic/ischaemic conditions. Clinically, anti-VEGF therapy has been shown to improve vision in diabetic maculopathy and in neovascular ARMD. The visual benefit in both conditions appears to arise from the restoration of BRB integrity with a reduction of retinal oedema.
血视网膜屏障（BRB）在视网膜微环境的稳态调节中起重要作用。它由内、外两部分组成，内血视网膜屏障（iBRB）由相邻视网膜毛细血管内皮细胞之间的紧密连接形成，外屏障（oBRB）由视网膜色素上皮细胞之间的紧密连接形成。星形胶质细胞、米勒细胞和周细胞有助于iBRB的正常功能。在许多临床上重要的病症中，包括糖尿病性视网膜病变、缺血性视网膜中央静脉阻塞和一些呼吸系统疾病，视网膜缺氧会导致iBRB的破坏。与血管通透性增加相关的iBRB破坏会导致血管源性水肿和组织损伤，从而对视力产生不利影响。血管内皮生长因子（VEGF）、一氧化氮（NO）、氧化应激和炎症等因素增加是iBRB通透性增加的基础，抑制这些因素是有益的。我们实验室的实验研究表明，褪黑素在缺氧条件下是iBRB的保护剂。虽然oBRB破坏可发生在加速性高血压和妊娠毒血症等病症中，这两种病症均与脉络膜缺血有关，以及年龄相关性黄斑变性（ARMD）中，并且是渗出性（浆液性）视网膜脱离的一个特征，但我们的研究表明，oBRB在缺氧/缺血条件下保持完整。临床上，抗VEGF治疗已被证明可改善糖尿病性黄斑病变和新生血管性ARMD患者的视力。这两种病症的视力改善似乎源于BRB完整性的恢复以及视网膜水肿的减轻。
