Triamcinolone Acetonide Protects Against Light-Induced Retinal Degeneration by Activating Anti-Inflammatory STAT6/Arg1 Signaling in Microglia

Excerpt

Retinal microglia are yolk sack-derived resident tissue macrophages in the retina [1]. Under normal conditions, microglia are localized to the retina outer plexiform layer (OPL) and inner plexiform layer (IPL), where they mediate homeostatic functions [2‐4]. During retinal degeneration, reactive microglia are detected in the degenerating photoreceptor layer, where they actively phagocytose viable photoreceptors, secrete proinflammatory cytokines, and induce chronic neuroinflammation, ultimately accelerating photoreceptor loss [5]. Consequently, inhibiting microglial activation is considered a potential treatment for retinal degenerative diseases, such as retinitis pigmentosa (RP) and age-related macular degeneration (AMD). Pharmacological inhibition of microglia activation has been shown to reduce photoreceptor death and improve retinal function [6‐8]. However, recent studies have also reported a protective role for microglia in retina. For example, microglia depletion accelerates photoreceptor death in response to light damage (LD) or retinal detachment [3, 9]. This protective effect of microglia may arise from a shift in their transcriptome toward a neuroprotective phenotype in specific locations, such as the subretinal space [3], or through the phagocytosis of injured retinal cell debris [9]. Therefore, the role of retinal microglia is highly dependent on the disease context. …