Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, USA.
Acta Ophthalmol. 2010 May;88(3):279-91. doi: 10.1111/j.1755-3768.2008.01501.x. Epub 2010 Mar 11.
Diabetic macular oedema (DMO) is an important cause of vision loss in patients with diabetes mellitus. The underlying mechanisms of DMO, on both macrocellular and microcellular levels, are discussed in this review. The pathophysiology of DMO can be described as a process whereby hyperglycaemia leads to overlapping and inter-related pathways that play a role not only in the initial vascular events, but also in the continued tissue insult that leads to chronic DMO. On a macrocellular level, DMO is believed to be in part caused by alterations in hydrostatic pressure, oxygen tension, oncotic pressure and shear stress. Three key components of the microvascular pathways include angiogenic factor expression, inflammation and oxidative stress. These molecular mediators, acting in conjunction with macrocellular factors, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, and leukostasis. The interactions, signalling events and feedback loops between the various molecules are complicated and are not completely understood. However, by attempting to understand the pathways involved in DMO, we can help guide new treatment options targeted towards specific factors or mediators.
糖尿病性黄斑水肿（DMO）是糖尿病患者视力丧失的重要原因。本综述讨论了 DMO 在宏观和微观水平上的潜在机制。DMO 的病理生理学可以描述为一个过程，其中高血糖导致重叠和相互关联的途径，不仅在初始血管事件中发挥作用，而且在导致慢性 DMO 的持续组织损伤中发挥作用。在宏观水平上，DMO 部分归因于静水压力、氧张力、胶体渗透压和剪切力的改变。微血管途径的三个关键组成部分包括血管生成因子表达、炎症和氧化应激。这些分子介质与宏观因素一起作用，部分受高血糖和缺氧的刺激，可直接对内皮细胞产生影响，导致通透性增加、血管内皮细胞连接中断和白细胞淤滞。各种分子之间的相互作用、信号事件和反馈环很复杂，尚未完全理解。然而，通过尝试了解 DMO 涉及的途径，我们可以帮助指导针对特定因素或介质的新治疗选择。
