缺血性中风相关神经血管单元的研究进展

Ibrain Pub Date : 2024-06-03 DOI:10.1002/ibra.12166
Yu Yang, Hao Tong, Zhuo‐Fan Ye, Zu‐Cai Xu, Tao Tao
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引用次数: 0

摘要

缺血性中风是临床上最常见的脑血管疾病。由于脑动脉血流中断、缺氧和局部脑组织缺血性坏死等多种因素,导致相关神经系统异常。神经血管单元(NVU)是一个动态的结构复合体,由神经元、神经胶质细胞、周细胞、血管内皮细胞和细胞外基质组成。在生理条件下,许多细胞共同维护中枢神经系统(CNS)的完整性。然而,缺血性中风后,随着组织缺血和缺氧的发展,以及 NVU 各成分之间相互作用的受损,NVU 的平衡被破坏。这些变化共同导致血脑屏障通透性增加、神经元功能障碍和神经传导束的功能性破坏,最终导致神经功能缺损的临床表现,包括运动、认知和语言障碍,阻碍康复进程。近年来,随着对缺血性脑血管病研究的不断深入,缺血性脑卒中中NVU不同细胞间的相互联系作用日益受到关注。为了阐述预防和治疗缺血性脑血管疾病的新概念,本文综述了缺血性中风发病机制中无损伤单元之间的相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Research progress of neurovascular units involved in ischemic stroke
Ischemic stroke is the most prevalent cerebrovascular disorder in the clinical setting. It results in associated neurological abnormalities due to a variety of factors, including disruption of cerebral arterial blood flow, hypoxia, and ischemic necrosis of local brain tissues. The neurovascular unit (NVU) is a dynamic structural complex that consists of neurons, glial cells, pericytes, vascular endothelial cells, and the extracellular matrix. Many cells work together to preserve the integrity of the central nervous system (CNS) under physiological conditions. However, following ischemic stroke, NVU homeostasis is disrupted along with the development of tissue ischemia and hypoxia, as well as impaired interactions between various components of the NVU. Collectively, the changes result in increased blood–brain barrier permeability, neuronal dysfunction, and functional destruction of nerve conduction bundles, ultimately leading to the clinical manifestation of neurological deficits including motor, cognitive, and speech impairments that hinder the rehabilitation process. In recent years, with continuously expanding research on ischemic cerebrovascular disease, the role of interconnections between different cells in the NVU in ischemic stroke has received increasing attention. To describe new concepts for the prevention and treatment of ischemic cerebrovascular illnesses, this article reviews the interplay between NVU in the pathogenesis of ischemic stroke.
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