Macrophage activation contributes to diabetic retinopathy

Zhang, Yi; Zhou, Aiyi

doi:10.1007/s00109-024-02437-5

Cited by 3 publications

(1 citation statement)

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“…The slow turnover of endothelial cells could explain the late onset and progressive development of RR. The role of retinal inflammation has been characterized in several retinal disorders, including diabetic retinopathy [8][9][10] and age-related macular degeneration (AMD) [11][12][13], but retinal inflammation after radiation has scarcely been explored, although clinical observations suggest that anti-inflammatory drugs such as corticosteroids may reduce RR manifestations [14]. In addition, the time course of glial and inflammatory cell activation has not been fully described, despite leukostasis being identified as an early pathogenic event [15], and whether retinal inflammation contributes to the microvascular damage occurring in RR remains uncertain.…”

Section: Introductionmentioning

confidence: 99%

Role of inflammation in a rat model of radiation retinopathy

Lebon,

Malaise,

Rimbert

et al. 2024

J Neuroinflammation

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Radiation retinopathy (RR) is a major side effect of ocular tumor treatment by plaque brachytherapy or proton beam therapy. RR manifests as delayed and progressive microvasculopathy, ischemia and macular edema, ultimately leading to vision loss, neovascular glaucoma, and, in extreme cases, secondary enucleation. Intravitreal anti-VEGF agents, steroids and laser photocoagulation have limited effects on RR. The role of retinal inflammation and its contribution to the microvascular damage occurring in RR remain incompletely understood. To explore cellular and vascular events after irradiation, we analyzed their time course at 1 week, 1 month and 6 months after rat eyes received 45 Gy X-beam photons. Müller glial cells, astrocytes and microglia were rapidly activated, and these markers of retinal inflammation persisted for 6 months after irradiation. This was accompanied by early cell death in the outer retina, which persisted at later time points, leading to retinal thinning. A delayed loss of small retinal capillaries and retinal hypoxia were observed after 6 months, indicating inner blood‒retinal barrier (BRB) alteration but without cell death in the inner retina. Moreover, activated microglial cells invaded the entire retina and surrounded retinal vessels, suggesting the role of inflammation in vascular alteration and in retinal cell death. Radiation also triggered early and persistent invasion of the retinal pigment epithelium by microglia and macrophages, contributing to outer BRB disruption. This study highlights the role of progressive and long-lasting inflammatory mechanisms in RR development and demonstrates the relevance of this rat model to investigate human pathology.

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