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Diabetic macular ischemia (DMI) is traditionally defined and graded on the angiographic evidence. However, these anatomical modifications are not surrogate markers for visual impairment. We suggest 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. Therefore, optical coherence tomography angiography (OCTA) is becoming the gold standard to identify the reversible DMI phenotypes. However, there is a need to standardize 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 edema. Finally, we discuss a complete set of proposed therapeutic pathways for DMI, including cell-based therapies that may provide restorative potential.
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Landini et al. (2023) studied this question.
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