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首页> 外文期刊>American Journal of Physiology >Enteric glia and neuroprotection: basic and clinical aspects
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Enteric glia and neuroprotection: basic and clinical aspects

机译：肠神经胶质和神经保护：基本和临床方面

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摘要

The enteric nervous system (ENS), a major regulatory system for gastrointestinal function, is composed of neurons and enteric glial cells (EGCs). Enteric glia have long been thought to provide only structural support to neurons. However, recent evidence indicates enteric glia-neuron cross talk significantly contributes to neuronal maintenance, survival, and function. Thus damage to EGCs may trigger neurodegenerative processes thought to play a role in gastrointestinal dysfunctions and symptoms. The purpose of this review is to provide an update on EGCs, particularly focusing on their possible neuroprotective features and the resultant enteric neuron abnormalities subsequent to EGC damage. These neuroprotective mechanisms may have pathogenetic relevance in a variety of functional and inflammatory gut diseases. Basic and clinical (translational) studies support a neuroprotective role mediated by EGCs. Different models have been developed to test whether selective EGC damage/ablation has an impact on gut functions and the ENS. Preclinical data indicated that selective EGC alterations were associated with changes in gut physiology related to enteric neuron abnormalities. In humans, a substantial loss of EGCs was described in patients with various functional and/or inflammatory gastrointestinal diseases. However, whether EGC changes precede or follow neuronal degeneration and loss and how this damage occurs is not defined. Additional studies on EGC neuroprotective capacity are expected to improve knowledge of gut diseases and pave the way for targeted therapeutic strategies of underlying neuropathies.
机译：肠神经系统（ENS）是胃肠道功能的主要调节系统，由神经元和肠神经胶质细胞（EGC）组成。长期以来，人们一直认为肠神经胶质只能为神经元提供结构性支持。但是，最近的证据表明，肠神经胶质神经元串扰显着促进了神经元的维持，存活和功能。因此，对EGC的损害可能会触发被认为在胃肠功能障碍和症状中起作用的神经退行性过程。这篇综述的目的是提供有关EGC的最新信息，特别是关注其可能的神经保护功能以及EGC损伤后导致的肠道神经元异常。这些神经保护机制可能在多种功能性和炎症性肠道疾病中具有致病性。基础和临床（翻译）研究支持由EGC介导的神经保护作用。已经开发出不同的模型来测试选择性EGC损伤/消融是否对肠道功能和ENS有影响。临床前数据表明，选择性EGC改变与肠道神经元异常相关的肠道生理变化有关。在人类中，患有各种功能性和/或炎性胃肠道疾病的患者描述了EGC的大量损失。但是，EGC变化是在神经元变性和丧失之前还是之后，以及这种损害的发生方式尚不确定。预期对EGC神经保护能力的其他研究将改善肠道疾病的知识，并为潜在的神经病的靶向治疗策略铺平道路。

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