Collyer Eileen, Blanco-Suarez Elena
Department of Neuroscience, Vickie and Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, PA, United States.
Front Mol Med. 2023 Sep 7;3:1240862. doi: 10.3389/fmmed.2023.1240862. eCollection 2023.
Stroke is a condition characterized by sudden deprivation of blood flow to a brain region and defined by different post-injury phases, which involve various molecular and cellular cascades. At an early stage during the acute phase, fast initial cell death occurs, followed by inflammation and scarring. This is followed by a sub-acute or recovery phase when endogenous plasticity mechanisms may promote spontaneous recovery, depending on various factors that are yet to be completely understood. At later time points, stroke leads to greater neurodegeneration compared to healthy controls in both clinical and preclinical studies, this is evident during the chronic phase when recovery slows down and neurodegenerative signatures appear. Astrocytes have been studied in the context of ischemic stroke due to their role in glutamate re-uptake, as components of the neurovascular unit, as building blocks of the glial scar, and synaptic plasticity regulators. All these roles render astrocytes interesting, yet understudied players in the context of stroke-induced neurodegeneration. With this review, we provide a summary of previous research, highlight astrocytes as potential therapeutic targets, and formulate questions about the role of astrocytes in the mechanisms during the acute, sub-acute, and chronic post-stroke phases that may lead to neurorestoration or neurodegeneration.
中风是一种以大脑区域血液供应突然中断为特征的病症，并由不同的损伤后阶段所定义，这些阶段涉及各种分子和细胞级联反应。在急性期的早期阶段，会迅速发生最初的细胞死亡，随后是炎症和瘢痕形成。接下来是亚急性期或恢复期，此时内源性可塑性机制可能会促进自发恢复，这取决于各种尚未完全了解的因素。在后期时间点，临床和临床前研究均表明，与健康对照相比，中风会导致更严重的神经退行性变，这在慢性期很明显，此时恢复减缓且神经退行性特征出现。由于星形胶质细胞在谷氨酸再摄取、作为神经血管单元的组成部分、作为胶质瘢痕的构成要素以及突触可塑性调节方面发挥作用，因此已在缺血性中风的背景下对其进行了研究。所有这些作用使星形胶质细胞成为中风诱导的神经退行性变背景下有趣但尚未得到充分研究的参与者。通过本综述，我们总结了先前的研究，强调星形胶质细胞作为潜在的治疗靶点，并提出了有关星形胶质细胞在中风后急性、亚急性和慢性期机制中作用的问题，这些机制可能导致神经修复或神经退行性变。
