W. K. Kellogg Eye Center, University of Michigan Medical School, Michigan, Ann Arbor, MI 48105, USA.
Curr Med Chem. 2013;20(26):3241-50. doi: 10.2174/09298673113209990027.
Diabetic retinopathy (DR), commonly classified as a microvascular complication of diabetes, is now recognized as a neurovascular complication or sensory neuropathy resulting from disruption of the neurovascular unit. Current therapies for DR target the vascular complication of the disease process, including neovascularization and diabetic macular edema. Since neurodegeneration is an early event in the pathogenesis of DR, it will be important to unravel the mechanisms that contribute to neuroretinal cell death in order to develop novel treatments for the early stages of DR. In this review we comment on how inflammation, the metabolic derangements associated with diabetes, loss of neuroprotective factors, and dysregulated glutamate metabolism may contribute to retinal neurodegeneration during diabetes. Promising potential therapies based on these specific aspects of DR pathophysiology are also discussed. Finally, we stress the importance of developing and validating new markers of visual function that can be used to shorten the duration of clinical trials and accelerate the delivery of novel treatments for DR to the public.
糖尿病性视网膜病变（DR）通常被归类为糖尿病的微血管并发症，但现在被认为是一种神经血管并发症或感觉神经病变，是由于神经血管单元的破坏所致。目前针对 DR 的治疗方法针对疾病过程中的血管并发症，包括新生血管形成和糖尿病性黄斑水肿。由于神经退行性变是 DR 发病机制中的早期事件，因此阐明导致神经视网膜细胞死亡的机制对于开发 DR 早期阶段的新疗法非常重要。在这篇综述中，我们评论了炎症、与糖尿病相关的代谢紊乱、神经保护因子的丧失以及谷氨酸代谢失调如何导致糖尿病期间的视网膜神经退行性变。还讨论了基于 DR 病理生理学这些特定方面的有希望的潜在治疗方法。最后，我们强调了开发和验证新的视觉功能标志物的重要性，这些标志物可用于缩短临床试验的持续时间，并加速将新的 DR 治疗方法推向公众。
