lncNEAT1 通过 ceRNA 网络调控细胞氧化应激损伤的机制与研究进展

Research progress on the mechanism of lncNEAT1 in regulating cellular oxidative stress via the ceRNA network

摘要

细胞氧化应激深度参与调控细胞增殖、炎症反应及程序性死亡(如凋亡、铁死亡、自噬)等关键病理生理过程。长链非编码 RNA 核旁斑组装转录本 1(nuclear paraspeckle assembly transcript 1, lncNEAT1)是细胞应激反应的关键调控因子，其表达受氧化应激诱导，同时又通过竞争性内源性 RNA(competitive endogenous RNA, ceRNA)等分子机制反馈调控氧化应激水平，二者间的双向调控关系构成疾病发生发展的关键环节。lncNEAT1 在调控氧化还原稳态过程中具有双重效应，呈现出取决于细胞类型和病理环境的加剧或改善效应。本文总结了氧化应激调控 lncNEAT1 表达，详细阐述了 lncNEAT1 通过 ceRNA 网络吸附微小 RNA(microRNA, miRNA)，进而调控活性氧(reactive oxygen species, ROS)生成、影响关键转录因子[如核因子 E2 相关因子 2(nuclear factor erythroid 2-related factor 2, Nrf2)、核因子 κB(nuclear factor-κB, NF-κB)、信号转导和转录激活因子-3(signal transducer and activator of transcription 3, STAT3)]活性及干预谷胱甘肽(glutathione, GSH)合成等通路，促进或改善氧化应激与细胞氧化损伤的机制与研究进展。深入理解 lncNEAT1 与氧化应激之间的调控网络，有望为心脑血管、神经、生殖系统等相关疾病的发病机制与靶向治疗提供新策略。

Abstract

Cellular oxidative stress plays critical roles in regulating key pathophysiological processes, including cell proliferation, inflammatory responses, and programmed cell death (e.g., apoptosis, ferroptosis, and autophagy). Recent studies have revealed that the long non-coding RNA nuclear paraspeckle assembly transcript 1(lncNEAT1) serves a pivotal function in cellular stress responses. The expression of lncNEAT1 is induced under oxidative stress; in turn, it modulates oxidative stress levels via molecular mechanisms such as the competitive endogenous RNA(ceRNA) pathway. This bidirectional regulatory interplay constitutes a pivotal link in disease development and progression. LncNEAT1 exerts a dual role in regulating redox homeostasis, either exacerbating or alleviating effects depending on the cell type and pathological context. This review outlines how oxidative stress regulates lncNEAT1 expression and details the mechanisms by which lncNEAT1 functions as a ceRNA to sponge microRNA(miRNA), thereby modulating oxidative stress and cellular damage. These mechanisms include regulating reactive oxygen species (ROS) production, modulating the activity of key transcription factors (e.g., Nrf2, NF-κB, STAT3), and interfering with glutathione(GSH) synthesis. A deeper insight into the regulatory network between lncNEAT1 and oxidative stress is expected to provide novel strategies for elucidating pathogenesis, identifying diagnostic biomarkers, and developing targeted therapies for oxidative stress-related diseases affecting the cardiovascular, cerebrovascular, nervous, and reproductive systems.

关键词

核旁斑组装转录本 1 / 氧化应激 / 竞争性内源性 RNA / 活性氧 / 核因子 E2 相关因子 2

Key words

lncNEAT1 / Oxidative stress / Competitive endogenous RNA / Reactive oxygen species / Nuclear factor erythroid 2-related factor 2

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基金资助

国家自然科学基金面上项目(82274573)

山东省自然科学基金(ZR2021MH255, 2023QE331)

山东省泰山学者工程项目(tsqn202103182)