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神经血管单元处的血管-神经元耦合与神经血管耦合:高血压的影响

Vasculo-Neuronal Coupling and Neurovascular Coupling at the Neurovascular Unit: Impact of Hypertension.

作者信息

Presa Jessica L, Saravia Flavia, Bagi Zsolt, Filosa Jessica A

机构信息

Department of Physiology, Medical College of Georgia, Augusta University, Augusta, GA, United States.

Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires and Instituto de Biología y Medicina Experimental, CONICET, Buenos Aires, Argentina.

出版信息

Front Physiol. 2020 Sep 25;11:584135. doi: 10.3389/fphys.2020.584135. eCollection 2020.

Abstract

Components of the neurovascular unit (NVU) establish dynamic crosstalk that regulates cerebral blood flow and maintain brain homeostasis. Here, we describe accumulating evidence for cellular elements of the NVU contributing to critical physiological processes such as cerebral autoregulation, neurovascular coupling, and vasculo-neuronal coupling. We discuss how alterations in the cellular mechanisms governing NVU homeostasis can lead to pathological changes in which vascular endothelial and smooth muscle cell, pericyte and astrocyte function may play a key role. Because hypertension is a modifiable risk factor for stroke and accelerated cognitive decline in aging, we focus on hypertension-associated changes on cerebral arteriole function and structure, and the molecular mechanisms through which these may contribute to cognitive decline. We gather recent emerging evidence concerning cognitive loss in hypertension and the link with vascular dementia and Alzheimer's disease. Collectively, we summarize how vascular dysfunction, chronic hypoperfusion, oxidative stress, and inflammatory processes can uncouple communication at the NVU impairing cerebral perfusion and contributing to neurodegeneration.

摘要

神经血管单元(NVU)的组成部分建立了动态的相互作用,调节脑血流量并维持脑内稳态。在此,我们描述了越来越多的证据表明,NVU的细胞成分参与了诸如脑自动调节、神经血管耦合和血管 - 神经元耦合等关键生理过程。我们讨论了控制NVU稳态的细胞机制的改变如何导致病理变化,其中血管内皮和平滑肌细胞、周细胞和星形胶质细胞的功能可能起关键作用。由于高血压是中风和衰老中认知能力加速下降的一个可改变的风险因素,我们重点关注高血压相关的脑小动脉功能和结构变化,以及这些变化可能导致认知能力下降的分子机制。我们收集了有关高血压中认知丧失以及与血管性痴呆和阿尔茨海默病的联系的最新证据。总的来说,我们总结了血管功能障碍、慢性灌注不足、氧化应激和炎症过程如何破坏NVU的通讯,损害脑灌注并导致神经退行性变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c1b/7546852/d658b1cc162d/fphys-11-584135-g001.jpg

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