Long non-coding RNAs in retinal neovascularization: current research and future directions

Retinal neovascularization (RNV) is an intractable pathological hallmark of numerous ocular blinding diseases, including diabetic retinopathy, retinal vein occlusion, and retinopathy of prematurity. However, current therapeutic methods have potential side effects and limited efficacy. Thus, further studies on the pathogenesis of RNV-related disorders and novel therapeutic targets are critically required. Long non-coding RNAs (lncRNAs) have various functions and participate in almost all biological processes in living cells, such as translation, transcription, signal transduction, and cell cycle control. In addition, recent research has demonstrated critical modulatory roles of various lncRNAs in RNV. In this review, we summarize current knowledge about the expression and regulatory functions of lncRNAs related to the progression of pathological RNV.

We searched databases such as PubMed and Web of Science to gather and review information from the published literature.

In general, lncRNA MEG3 attenuates RNV, thus protecting the retina from excessive and dysregulated angiogenesis under high glucose stress. In contrast, lncRNAs MALAT1, MIAT, ANRIL, HOTAIR, HOTTIP, and SNHG16, have been identified as causative molecules in the pathological progression of RNV. Comprehensive and in-depth studies of the roles of lncRNAs in RNV indicate that targeting lncRNAs may be an alternative therapeutic approach in the near future, enabling new options for attenuating RNV progression and treating RNV-related retinal diseases.