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miR-34a 在神经生理学和神经病理学中的作用。

miR-34a in Neurophysiology and Neuropathology.

机构信息

Singapore Nuclear Research and Safety Initiative, National University of Singapore, Singapore, Singapore.

Department of Biochemistry, Yong Loo Lin School of Medicine, National University Health System, Singapore, Singapore.

出版信息

J Mol Neurosci. 2019 Feb;67(2):235-246. doi: 10.1007/s12031-018-1231-y. Epub 2018 Nov 28.

Abstract

Epigenetic influence of brain and neuronal function plays key regulatory roles in health and diseases. The microRNA miR-34a is a tumor suppressor transcript, and its loss has been prominently linked to various human cancers, including malignancies of the brain. Interestingly, miR-34a is abundantly expressed in the adult mammalian brain, and emerging evidence has implicated its involvement in a range of neurodevelopmental and neuropathological processes. Developmentally, miR-34a regulates neural stem/progenitor cell differentiation and aspects of neurogenesis. During aging, its elevation is connected to hearing loss and age-related macular degeneration. Pathologically, its elevations during epileptic seizures and ischemic stroke contribute to neuronal injury and death. Inhibition or suppression of miR-34a improved neuronal survival against a variety of neurotoxins implicated in Parkinson's disease. Its elevation may also play a role in neuronal demise in animal models of Alzheimer's disease, and suppression of its levels may be generally neuroprotective. The roles and activities of miR-34a in the brain are modulated by factors that control its expression (such as Tp53/73), as well as its downstream target genes (such as the sirtuins SIRT1 and SIRT6) and signaling pathways (such the Notch pathway). We discuss here the known and emerging roles of the miR-34a regulatory network in neurophysiology and neuropathology.

摘要

脑和神经元功能的表观遗传影响在健康和疾病中起着关键的调节作用。microRNA miR-34a 是一种肿瘤抑制转录物,其缺失与各种人类癌症密切相关,包括脑部恶性肿瘤。有趣的是,miR-34a 在成年哺乳动物脑中大量表达,新出现的证据表明其参与了一系列神经发育和神经病理过程。在发育过程中,miR-34a 调节神经干细胞/祖细胞的分化和神经发生的各个方面。在衰老过程中,其升高与听力损失和年龄相关性黄斑变性有关。在病理上,其在癫痫发作和缺血性中风期间的升高导致神经元损伤和死亡。抑制或抑制 miR-34a 可改善多种与帕金森病相关的神经毒素引起的神经元存活。其升高也可能在阿尔茨海默病的动物模型中导致神经元死亡,而抑制其水平通常具有神经保护作用。控制其表达(如 Tp53/73)的因素以及其下游靶基因(如 sirtuins SIRT1 和 SIRT6)和信号通路(如 Notch 通路)调节 miR-34a 在大脑中的作用和活性。我们在这里讨论了 miR-34a 调控网络在神经生理学和神经病理学中的已知和新兴作用。

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