Apoptosis and long non-coding RNAs: Focus on their roles in ischemic stroke

IF 2.7 4区医学 Q3 NEUROSCIENCES

Brain Research Pub Date : 2024-11-22 DOI:10.1016/j.brainres.2024.149346

Jia Min Ding , Hui Min Zhong , Kuan Huang , Wen Zeng , Li Chen

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引用次数: 0

Abstract

Ischemic stroke (IS) is a severe and sudden cerebrovascular event, associated with notably high rates of mortality and morbidity. The process of apoptosis, a genetically orchestrated form of programmed cell death, is divided into two pathways: intrinsic and extrinsic. The intricate involvement of long non-coding RNA (lncRNA) in the pathobiology of IS, particularly in modulating neuronal apoptosis, is a burgeoning area of research. This review synthesizes the current understanding of the regulatory mechanisms of lncRNA on neuronal apoptosis in the context of ischemic stroke. Specifically, we highlight the roles of lncRNA such as ANRIL, C2dat1/2, H19, TUG1, MEG3, SNHG, and GAS5, which have been implicated in the facilitation of neuronal apoptosis. Conversely, the lncRNA N1LR has been shown to exert an inhibitory effect on this process. The role of MALAT1 in neuronal apoptosis remains a subject of ongoing debate, as its function oscillates between pro-apoptotic and anti-apoptotic roles, thus highlighting the need for further elucidation.

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细胞凋亡和长非编码 RNA：关注它们在缺血性中风中的作用。

缺血性中风（IS）是一种严重的突发性脑血管事件，死亡率和发病率都很高。细胞凋亡是一种由基因精心策划的细胞程序性死亡，其过程分为内在和外在两种途径。长非编码 RNA（lncRNA）在 IS 的病理生物学中的复杂参与，特别是在调节神经元凋亡方面，是一个新兴的研究领域。本文综述了目前对缺血性脑卒中中 lncRNA 对神经细胞凋亡调控机制的认识。具体而言，我们强调了 lncRNA 的作用，如 ANRIL、C2dat1/2、H19、TUG1、MEG3、SNHG 和 GAS5，它们与神经元凋亡的促进作用有牵连。相反，lncRNA N1LR 则被证明对这一过程有抑制作用。MALAT1 在神经元凋亡中的作用仍是一个争论不休的问题，因为它的功能在促凋亡和抗凋亡作用之间摇摆，因此需要进一步阐明。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Brain Research 医学-神经科学

CiteScore

5.90

自引率

3.40%

发文量

268

审稿时长

47 days

期刊介绍： An international multidisciplinary journal devoted to fundamental research in the brain sciences. Brain Research publishes papers reporting interdisciplinary investigations of nervous system structure and function that are of general interest to the international community of neuroscientists. As is evident from the journals name, its scope is broad, ranging from cellular and molecular studies through systems neuroscience, cognition and disease. Invited reviews are also published; suggestions for and inquiries about potential reviews are welcomed. With the appearance of the final issue of the 2011 subscription, Vol. 67/1-2 (24 June 2011), Brain Research Reviews has ceased publication as a distinct journal separate from Brain Research. Review articles accepted for Brain Research are now published in that journal.