Noncoding RNAs as a novel approach to target retinopathy of prematurity

Author:

Kim Hyunjong,Kim Jaesub,Ryu Juhee

Abstract

Retinopathy of prematurity (ROP), a vascular disease characterized by abnormal vessel development in the retina, has become a primary cause of blindness in children around the world. ROP can be developed during two different phases: vessel loss and vessel proliferation. Once preterm infants with immature retinal vessel growth are exposed to high level of oxygen inside the incubator, vessel loss can occur. When infants are exposed to room air, they may experience the proliferation of vessels in the retina. Although multiple factors are reported to be involved in the pathogenesis of ROP, including vaso-endothelial growth factors (VEGFs) and hypoxia-inducible factors, the pathogenesis of ROP is not completely understood. Although laser therapy and pharmacologic agents, such as anti-VEGF agents, have been commonly used to treat ROP, the incidence of ROP is rapidly rising. Given that current therapies can be invasive and long-term effects are not fully known, the search for novel therapeutic targets with less destructive properties needs to be considered. Within the last decade, the field of noncoding RNA therapy has shown potential as next-generation therapy to treat diverse diseases. In this review, we introduce various noncoding RNAs regulating ROP and discuss their role as potential therapeutic targets in ROP.

Funder

National Research Foundation of Korea

Publisher

Frontiers Media SA

Subject

Pharmacology (medical),Pharmacology

Cited by 3 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. m6A-Mediated Upregulation of Imprinted in Prader–Willi Syndrome Induces Aberrant Apical–Basal Polarization and Oxidative Damage in RPE Cells;Investigative Opthalmology & Visual Science;2024-02-05

2. Systemic Cytokines in Retinopathy of Prematurity;Journal of Personalized Medicine;2023-02-05

3. MicroRNAs in the Mouse Developing Retina;International Journal of Molecular Sciences;2023-02-03

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