Progress in Retinal and Eye Research ( IF 17.8 ) Pub Date : 2021-12-11 , DOI: 10.1016/j.preteyeres.2021.101033 Chui Ming Gemmy Cheung 1 , Amani Fawzi 2 , Kelvin Yc Teo 3 , Hisashi Fukuyama 4 , Sagnik Sen 5 , Wei-Shan Tsai 6 , Sobha Sivaprasad 6
Diabetic macular ischaemia (DMI) is traditionally defined and graded based on the angiographic evidence of an enlarged and irregular foveal avascular zone. However, these anatomical changes are not surrogate markers for visual impairment. We postulate that there are vascular phenotypes of DMI based on the relative perfusion deficits of various retinal capillary plexuses and choriocapillaris. This review highlights several mechanistic pathways, including the role of hypoxia and the complex relation between neurons, glia, and microvasculature. The current animal models are reviewed, with shortcomings noted. Therefore, utilising the advancing technology of optical coherence tomography angiography (OCTA) to identify the reversible DMI phenotypes may be the key to successful therapeutic interventions for DMI. However, there is a need to standardise the nomenclature of OCTA perfusion status. Visual acuity is not an ideal endpoint for DMI clinical trials. New trial endpoints that represent disease progression need to be developed before irreversible vision loss in patients with DMI. Natural history studies are required to determine the course of each vascular and neuronal parameter to define the DMI phenotypes. These DMI phenotypes may also partly explain the development and recurrence of diabetic macular oedema. It is also currently unclear where and how DMI fits into the diabetic retinopathy severity scales, further highlighting the need to better define the progression of diabetic retinopathy and DMI based on both multimodal imaging and visual function. Finally, we discuss a complete set of proposed therapeutic pathways for DMI, including cell-based therapies that may provide restorative potential.
中文翻译:
糖尿病性黄斑缺血——新的治疗靶点?
糖尿病性黄斑缺血 (DMI) 传统上是根据扩大和不规则中心凹无血管区的血管造影证据来定义和分级的。然而,这些解剖学变化并不是视力障碍的替代标志。我们假设存在基于各种视网膜毛细血管丛和脉络膜毛细血管的相对灌注不足的 DMI 血管表型。这篇综述重点介绍了几种机制途径,包括缺氧的作用以及神经元、神经胶质和微血管系统之间的复杂关系。审查了当前的动物模型,并指出了不足之处。因此,利用先进的光学相干断层扫描血管造影(OCTA)技术来识别可逆的 DMI 表型可能是 DMI 成功治疗干预的关键。然而,有必要对 OCTA 灌注状态的命名进行标准化。视力不是 DMI 临床试验的理想终点。代表疾病进展的新试验终点需要在 DMI 患者出现不可逆转的视力丧失之前制定。需要自然史研究来确定每个血管和神经元参数的过程,以定义 DMI 表型。这些 DMI 表型也可以部分解释糖尿病黄斑水肿的发生和复发。目前还不清楚 DMI 在何处以及如何适合糖尿病视网膜病变严重程度量表,进一步强调需要根据多模态成像和视觉功能更好地定义糖尿病视网膜病变和 DMI 的进展。最后,我们讨论了一整套建议的 DMI 治疗途径,