The role of inflammation and neurodegeneration in diabetic macular edema

The pathogenesis of diabetic macular edema (DME) is complex. Persistently high blood glucose activates multiple cellular pathways and induces inflammation, oxidation stress, and vascular dysfunction. Retinal ganglion cells, macroglial and microglial cells, endothelial cells, pericytes, and retinal pigment epithelium cells are involved. Neurodegeneration, characterized by dysfunction or apoptotic loss of retinal neurons, occurs early and independently from the vascular alterations. Despite the increasing knowledge on the pathways involved in DME, only limited therapeutic strategies are available. Besides antiangiogenic drugs and intravitreal corticosteroids, alternative therapeutic options tackling inflammation, oxidative stress, and neurodegeneration have been considered, but none of them has been currently approved.

Automated summary

The pathogenesis of diabetic macular edema (DME) is complex and involves multiple factors such as inflammation, oxidative stress, and vascular dysfunction, along with early neurodegenerative changes. Despite increasing knowledge on the pathways involved in DME, therapeutic options are limited, with antiangiogenic drugs and intravitreal corticosteroids being the main choices currently available. Alternative therapeutic options targeting inflammation, oxidative stress, and neurodegeneration are being considered, but none have been approved yet.