Abstract
Microglia have been implicated in many degenerative eye disorders, including retinitis pigmentosa, age-related macular degeneration, glaucoma, diabetic retinopathy, uveitis, and retinal detachment. While the exact roles of microglia in these conditions are still being discovered, evidence from animal models suggests that they can modulate the course of disease. In this review, we highlight current strategies to target microglia in the eye and their potential as treatments for both rare and common ocular disorders. These approaches include depleting microglia with chemicals or radiation, reprogramming microglia using homeostatic signals or other small molecules, and inhibiting the downstream effects of microglia such as by blocking cytokine activity or phagocytosis. Finally, we describe areas of future research needed to fully exploit the therapeutic value of microglia in eye diseases.
Highlights
First described by Pıó del Rıó -Hortega in the early 20th century, microglia are the resident immune cells of the central nervous system (CNS), including the retina
Microglia have been implicated in the progression of retinitis pigmentosa (RP), age-related macular degeneration (AMD), glaucoma, diabetic retinopathy (DR), uveitis, and retinal detachment among other ocular conditions [14,15,16,17,18,19] (Figure 1). While these diseases differ in their underlying etiologies, they are all characterized by the loss of photoreceptors or retinal ganglion cells (RGCs), resulting in deterioration of vision and, in some cases, blindness
RGC survival in these animals was improved by NLY01, a glucagon-like peptide 1 receptor (GLP1R) agonist that has been shown to halt astrocyte transformation by suppressing microglial expression of IL-1a, tumor necrosis factor (TNF), and component 1q (C1q) [100, 101]
Summary
First described by Pıó del Rıó -Hortega in the early 20th century, microglia are the resident immune cells of the central nervous system (CNS), including the retina. Targeting Microglia in Eye Disease microglia could alleviate photoreceptor and RGC death, thereby helping patients preserve their sight. Only irradiated eyes showed reduced expression of IBA1 [36, 37], a marker for microglia, suggesting that depletion of microglia may have contributed to saving RGCs. Outside of DBA/2J mice, low-dose gamma radiation has been found to delay photoreceptor death in both the rd1 and rd10 models of RP [38].
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