Diabetic retinal neurodegeneration (DRN) is a condition in which the normal function of retinal neurovascular units is impaired due to various factors such as oxidative stress, microvascular damage, metabolic disorders, neurotrophic factor imbalance, and immune damage in hyperglycemia environment. The loss of neurons and glial dysfunction is involved in the destruction of the blood-retinal barrier, impaired vascular response and neurovascular coupling, leading to microvascular disease and neurodegeneration. More and more studies have proved that DRN is associated with microangiopathy and diabetic retinopathy pathogenesis. A deeper understanding of the pathogenesis of neurovascular injury may provide new and more effective prevention strategies for diabetic retinopathy.
Retinopathy of prematurity (ROP) is a retinal vascular disease in preterm or low birth weight infants and a leading cause of childhood blindness. Anti-vascular endothelial growth factor (VEGF) therapy offers advantages such as minimal invasiveness and convenient intervention; however, it carries a relatively high risk of disease reactivation, necessitating long-term follow-up due to the potential for severe outcomes. Studies indicate that post-anti-VEGF reactivation rates vary regionally and are related with birth status, ROP severity, and the specific anti-VEGF agent used. Most reactivations occur 6-16 weeks after initial treatment, at a postmenstrual age of 37-60 weeks. Reactivated lesions often develop at the original ridge or the junction of vascularized and avascular retina, and may present with dilation and tortuosity of the posterior retinal vessels, peripheral vascular leakage, neovascularization, or retinal detachment. Fundus fluorescein angiography may reveal Plus disease, posterior arterial tortuosity, abnormal nondichotomous retinal vessel branching at the junction of vascularized and avascular retina, irregular circumferential vessels, vasoobliteration with capillary nonperfusion, neovascularization, and fluorescein leakage. The choice of retreatment (such as retinal laser photocoagulation, intravitreal anti-VEGF injection, or vitrectomy) should be decided by the timing and severity of reactivation, along with prognostic considerations. It is recommended to establish a standardized management protocol for reactivation after anti-VEGF treatment in ROP to enable early detection and intervention, thereby preventing severe visual impairment. Future studies should focus on the mechanisms underlying ROP reactivation, differences in reactivation rates and timing among various anti-VEGF agents, predictive models for reactivation risk, and long-term management of reactivated disease.