The incidence of progressive neovascular retinopathies (NRs) that result in progressive vision loss is expected to increase by ~33% in adults of developed nations by 2030, including the United States and United Kingdom [1,2,3,4,5]. Antiangiogenic treatments, such as Lucentis® (ranibizumab), Avastin® (bevacizumab) and Eylea® (aflibercept), have demonstrated their efficacy in improving the visual acuity (VA) of patients suffering of NRs while undergoing treatment [6, 7]. However, declining VA in patients and increased prevalence of retinal scarring, post-treatment, have raised concerns [8, 9]. Although contemporary antiangiogenic treatments have aimed to decelerate the progression of NRs, retinal scarring developed as a consequence of aberrant angiogenesis remains a primary, and understudied, factor in irreversible vision loss.

Müller glia (MG) respond to retinal insult via reactive gliosis, a group of processes that regulate changes in their cellular and molecular behaviour. Although initial MG gliosis is neuroprotective, the prolonged dysregulation of retinal homoeostasis as a result of NRs leads to disruptive behaviours and subsequent glial scar formation. Emerging therapies that address the progression of gliosis from aberrant angiogenesis will thereby target scarring as a separate, contributing factor to vision loss from NRs.

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