The study emphasized a number of mechanistic pathways, including the significance of hypoxia and the nuanced interactions between neurons, glia, and microvasculature. There are issues with the present animal models that were reviewed. Based on the relative perfusion deficits of different retinal capillary plexuses and choriocapillaris, researchers hypothesized that Diabetic muscle infarction (DMI) manifests as different vascular phenotypes. This study emphasized a number of mechanistic pathways, including the significance of hypoxia and the nuanced interactions between neurons, glia, and microvasculature. There were issues with the present animal models that were reviewed. In order to effectively treat DMI, it may be necessary to use the developing technique of optical coherence tomography angiography (OCTA) to detect the reversible DMI phenotypes. But the nomenclature for OCTA perfusion status needs to be standardized. For DMI clinical trials, visual acuity was not a good endpoint. Prior to patients with DMI losing their eyesight permanently, new trial endpoints that reflect disease progression must be created. In order to identify the DMI phenotypes, natural history studies were necessary to ascertain how each vascular and neural parameter evolves over time. Additionally, the development and recurrence of diabetic macular edema may be partially explained by these DMI characteristics. Additionally, it was still unclear where and how DMI fits into the diabetic retinopathy severity scales, emphasizing the need for a clearer definition of the progression of DMI based on multimodal imaging and visual function as well as diabetic retinopathy. Investigators concluded by going over a comprehensive list of suggested therapy routes for DMI, including cell-based treatments with promise for restoration.
Source: sciencedirect.com/science/article/abs/pii/S135094622100094X
