lncNEAT1通过ceRNA网络调控细胞氧化应激损伤的机制与研究进展

doi:10.6040/j.issn.1671-7554.0.2025.1132

摘要/Abstract

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(glutathion, 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。

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

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.

Key words: lncNEAT1, Oxidative stress, Competitive endogenous RNA, Reactive oxygen species, Nuclear factor erythroid 2-related factor 2

中图分类号:

R329.2

张翰之,陈雯,梁启惠,丁胜勇,吴海萃. lncNEAT1通过ceRNA网络调控细胞氧化应激损伤的机制与研究进展[J]. 山东大学学报 (医学版), 2026, 64(7): 100-117.

ZHANG Hanzhi, CHEN Wen, LIANG Qihui, DING Shengyong, WU Haicui. Research progress on the mechanism of lncNEAT1 in regulating cellular oxidative stress via the ceRNA network[J]. Journal of Shandong University (Health Sciences), 2026, 64(7): 100-117.

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