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靶向泡沫细胞形成以改善缺血性中风的恢复。

Targeting foam cell formation to improve recovery from ischemic stroke.

机构信息

Department of Immunobiology, University of Arizona, United States.

Department of Pediatrics, University of Arizona, United States.

出版信息

Neurobiol Dis. 2023 Jun 1;181:106130. doi: 10.1016/j.nbd.2023.106130. Epub 2023 Apr 15.

DOI:10.1016/j.nbd.2023.106130
PMID:37068641
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10993857/
Abstract

Inflammation is a crucial part of the healing process after an ischemic stroke and is required to restore tissue homeostasis. However, the inflammatory response to stroke also worsens neurodegeneration and creates a tissue environment that is unfavorable to regeneration for several months, thereby postponing recovery. In animal models, inflammation can also contribute to the development of delayed cognitive deficits. Myeloid cells that take on a foamy appearance are one of the most prominent immune cell types within chronic stroke infarcts. Emerging evidence indicates that they form as a result of mechanisms of myelin lipid clearance becoming overwhelmed, and that they are a key driver of the chronic inflammatory response to stroke. Therefore, targeting lipid accumulation in foam cells may be a promising strategy for improving recovery. The aim of this review is to provide an overview of current knowledge regarding inflammation and foam cell formation in the brain in the weeks and months following ischemic stroke and identify targets that may be amenable to therapeutic intervention.

摘要

炎症是缺血性中风后修复过程的关键部分,对于恢复组织内稳态是必需的。然而,中风后的炎症反应也会加重神经退行性病变,并在几个月内产生不利于再生的组织环境,从而延迟恢复。在动物模型中,炎症也可能导致认知障碍的延迟发生。在慢性中风梗死灶中,外观呈泡沫状的髓样细胞是最突出的免疫细胞类型之一。新出现的证据表明,它们是髓磷脂脂质清除机制不堪重负的结果,是中风后慢性炎症反应的关键驱动因素。因此,针对泡沫细胞中的脂质积累可能是改善恢复的一种有前途的策略。本综述的目的是提供一个关于缺血性中风后数周和数月内大脑炎症和泡沫细胞形成的最新知识概述,并确定可能适合治疗干预的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f89/10993857/e8bfeff82b3f/nihms-1979923-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f89/10993857/a66f582037ab/nihms-1979923-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f89/10993857/58ff34f85532/nihms-1979923-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f89/10993857/e8bfeff82b3f/nihms-1979923-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f89/10993857/a66f582037ab/nihms-1979923-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f89/10993857/58ff34f85532/nihms-1979923-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f89/10993857/e8bfeff82b3f/nihms-1979923-f0003.jpg

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本文引用的文献

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Int Immunopharmacol. 2022 Aug;109:108733. doi: 10.1016/j.intimp.2022.108733. Epub 2022 May 4.
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Stroke induces disease-specific myeloid cells in the brain parenchyma and pia.中风会在脑实质和脑膜中诱导出具有疾病特异性的髓样细胞。
Nat Commun. 2022 Feb 17;13(1):945. doi: 10.1038/s41467-022-28593-1.
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Recent Progress in Models for Atherosclerosis Studies.动脉粥样硬化研究模型的最新进展
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Assessment and Quantification of Foam Cells and Lipid Droplet-Accumulating Microglia in Mouse Brain Tissue Using BODIPY Staining.使用硼二吡咯甲川(BODIPY)染色法对小鼠脑组织中的泡沫细胞和脂质小滴聚集的小胶质细胞进行评估和定量分析。
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Chronic consequences of ischemic stroke: Profiling brain injury and inflammation in a mouse model with reperfusion.缺血性中风的慢性后果:再灌注小鼠模型中的脑损伤和炎症特征分析。
Physiol Rep. 2024 Jun;12(12):e16118. doi: 10.14814/phy2.16118.
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