Hippo信号通路作为阿尔茨海默病的治疗靶点

IF 17.5 1区 医学 Q1 NEUROSCIENCES
Doris Chen, Stella Wigglesworth-Littlewood, Frank J. Gunn-Moore
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引用次数: 0

摘要

Hippo信号通路因其调节器官大小、细胞增殖、细胞凋亡以及细胞迁移和分化而闻名。最近的研究表明,Hippo信号在神经系统中也起着重要作用,参与神经炎症、神经元分化和神经元死亡和变性。因此,Hippo信号的失调,特别是其核心激酶MST1/2和LATS1/2的失调,已经开始引起阿尔茨海默病(AD)领域的关注。在这里,我们通过概述Hippo信号在神经系统中的功能、在AD患者和模型中其失调的证据,以及最近涉及该通路在AD中的遗传或药理学调节的研究,讨论了靶向Hippo通路在AD中的治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Hippo signaling pathway as a therapeutic target in Alzheimer’s disease
The Hippo signaling pathway is well-known for its regulation of organ size, cell proliferation, apoptosis, and cell migration and differentiation. Recent studies have demonstrated that Hippo signaling also plays important roles in the nervous system, being involved in neuroinflammation, neuronal differentiation, and neuronal death and degeneration. As such, dysregulation of Hippo signaling, particularly of its core kinases MST1/2 and LATS1/2, has begun to attract attention in the Alzheimer’s disease (AD) field. Here, we discuss the therapeutic potential of targeting the Hippo pathway in AD by providing an overview of Hippo signaling with regards to its function in the nervous system, evidence for its dysregulation in AD patients and models, and recent studies involving genetic or pharmacological modulation of this pathway in AD.
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来源期刊
Molecular Neurodegeneration
Molecular Neurodegeneration 医学-神经科学
CiteScore
23.00
自引率
4.60%
发文量
78
审稿时长
6-12 weeks
期刊介绍: Molecular Neurodegeneration, an open-access, peer-reviewed journal, comprehensively covers neurodegeneration research at the molecular and cellular levels. Neurodegenerative diseases, such as Alzheimer's, Parkinson's, Huntington's, and prion diseases, fall under its purview. These disorders, often linked to advanced aging and characterized by varying degrees of dementia, pose a significant public health concern with the growing aging population. Recent strides in understanding the molecular and cellular mechanisms of these neurodegenerative disorders offer valuable insights into their pathogenesis.
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