Abstract
The leading cause of central vision loss, age‐related macular degeneration (AMD), is a degenerative disorder characterized by atrophy of retinal pigment epithelium (RPE) and photoreceptors. For 15% of cases, neovascularization occurs, leading to acute vision loss if left untreated. For the remaining patients, there are currently no treatment options and preventing progressive RPE atrophy remains the main therapeutic goal. Previously, we have shown treatment with interleukin‐33 can reduce choroidal neovascularization and attenuate tissue remodelling. Here, we investigate IL‐33 delivery in aged, high‐fat diet (HFD) fed mice on a wildtype and complement factor H heterozygous knockout background. We characterize the non‐toxic effect following intravitreal injection of IL‐33 and further demonstrate protective effects against RPE cell death with evidence of maintaining metabolic retinal homeostasis of Cfh+/−~HFD mice. Our results further support the potential utility of IL‐33 to prevent AMD progression.
Highlights
Age-related macular degeneration (AMD) is a degenerative disease of the eye and the leading cause of central vision loss
Characterized by drusen deposits, atrophy of the retinal pigment epithelium (RPE) and photoreceptor (PR) loss, AMD can progress into two stages of vision loss, acute neovascularization AMD and, in the majority of patients, pernicious geographic atrophy
We previously revealed a protective role for interleukin-33 (IL-33), in choroidal neovascularization and attenuation of wound healing.[3]
Summary
Age-related macular degeneration (AMD) is a degenerative disease of the eye and the leading cause of central vision loss. We use an insidious aAMD model, aged heterozygous complement factor H knockout (Cfh+/−) mice on a high-fat diet (HFD)[6] to determine the safety of IL-33 treatment and demonstrate its potential as an early therapeutic for preventing AMD progression. The Cfh+/−~HFD model presents with distinct disease phenotype, without significant cell loss,[6] providing opportunity to measure treatment toxicity and efficacy in a mimic of early/intermediate aAMD.
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