Beyond Neovascularization: Light Response Deficits in Oxygen-Induced Retinopathy Models

Retinopathy of prematurity (ROP) has traditionally been viewed as a retinal vascular disease. However, even after vascular recovery, many patients experience retinal light response deficits for years, possibly lifelong. Despite major treatment advances that target abnormal retinal neovascularization, ROP remains a major cause of vision loss in premature infants. The mouse and rat oxygen-induced retinopathy (OIR) models are widely used to study ROP and have been instrumental in developing anti-VEGF treatments for retinal neovascular diseases. In contrast, the mechanisms underlying retinal light response deficits in ROP remain poorly understood-and this limits the development of therapies targeting the neuronal component of ROP. This review summarizes current knowledge of retinal light response deficits in OIR across different retinal cell populations. Available evidence suggests that deficits originate in photoreceptors and propagate through downstream retinal neurons, resulting in cumulative impairment across the retinal circuit. By reviewing existing findings, discussing underlying mechanisms, and identifying key knowledge gaps, this review evaluates OIR as a valuable platform to investigate retinal light response deficits and to guide the development of strategies to improve long-term vision outcomes for patients with ROP.