Cerebral Hypoxia-Induced Molecular Alterations and Their Impact on the Physiology of Neurons and Dendritic Spines: A Comprehensive Review.

IF 3.6 4区 医学 Q3 CELL BIOLOGY
Chao Cui, Xue Jiang, Yumei Wang, Chao Li, Zhaochen Lin, Youzhen Wei, Qingbin Ni
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引用次数: 0

Abstract

This article comprehensively reviews how cerebral hypoxia impacts the physiological state of neurons and dendritic spines through a series of molecular changes, and explores the causal relationship between these changes and neuronal functional impairment. As a severe pathological condition, cerebral hypoxia can significantly alter the morphology and function of neurons and dendritic spines. Specifically, dendritic spines, being the critical structures for neurons to receive information, undergo changes such as a reduction in number and morphological abnormalities under hypoxic conditions. These alterations further affect synaptic function, leading to neurotransmission disorders. This article delves into the roles of molecular pathways like MAPK, AMPA receptors, NMDA receptors, and BDNF in the hypoxia-induced changes in neurons and dendritic spines, and outlines current treatment strategies. Neurons are particularly sensitive to cerebral hypoxia, with their apical dendrites being vulnerable to damage, thereby affecting cognitive function. Additionally, astrocytes and microglia play an indispensable role in protecting neuronal and synaptic structures, regulating their normal functions, and contributing to the repair process following injury. These studies not only contribute to understanding the pathogenesis of related neurological diseases but also provide important insights for developing novel therapeutic strategies. Future research should further focus on the dynamic changes in neurons and dendritic spines under hypoxic conditions and their intrinsic connections with cognitive function.

Abstract Image

脑缺氧诱导的分子变化及其对神经元和树突棘生理的影响:全面综述》。
本文全面回顾了脑缺氧如何通过一系列分子变化影响神经元和树突棘的生理状态,并探讨了这些变化与神经元功能损伤之间的因果关系。作为一种严重的病理状态,脑缺氧会显著改变神经元和树突棘的形态和功能。具体而言,树突棘是神经元接收信息的关键结构,在缺氧条件下会发生变化,如数量减少和形态异常。这些变化会进一步影响突触功能,导致神经传递失调。本文深入探讨了 MAPK、AMPA 受体、NMDA 受体和 BDNF 等分子通路在缺氧诱导的神经元和树突棘变化中的作用,并概述了当前的治疗策略。神经元对脑缺氧特别敏感,其顶端树突易受损,从而影响认知功能。此外,星形胶质细胞和小胶质细胞在保护神经元和突触结构、调节其正常功能以及促进损伤后的修复过程中发挥着不可或缺的作用。这些研究不仅有助于了解相关神经疾病的发病机制,还为开发新型治疗策略提供了重要见解。未来的研究应进一步关注缺氧条件下神经元和树突棘的动态变化及其与认知功能的内在联系。
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
CiteScore
7.70
自引率
0.00%
发文量
137
审稿时长
4-8 weeks
期刊介绍: Cellular and Molecular Neurobiology publishes original research concerned with the analysis of neuronal and brain function at the cellular and subcellular levels. The journal offers timely, peer-reviewed articles that describe anatomic, genetic, physiologic, pharmacologic, and biochemical approaches to the study of neuronal function and the analysis of elementary mechanisms. Studies are presented on isolated mammalian tissues and intact animals, with investigations aimed at the molecular mechanisms or neuronal responses at the level of single cells. Cellular and Molecular Neurobiology also presents studies of the effects of neurons on other organ systems, such as analysis of the electrical or biochemical response to neurotransmitters or neurohormones on smooth muscle or gland cells.
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