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缺血性脑卒中的新型治疗策略:自噬的最新研究进展。

Novel Therapeutic Strategies for Ischemic Stroke: Recent Insights into Autophagy.

机构信息

Department of Neurosurgery, Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.

Department of Neurosurgery, The Affiliated Suqian Hospital of Xuzhou Medical University, No.138, Huanghe South Road, Suqian, 223800 Jiangsu, China.

出版信息

Oxid Med Cell Longev. 2022 Jun 8;2022:3450207. doi: 10.1155/2022/3450207. eCollection 2022.

DOI:10.1155/2022/3450207
PMID:35720192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9200548/
Abstract

Stroke is one of the leading causes of death and disability worldwide. Autophagy is a conserved cellular catabolic pathway that maintains cellular homeostasis by removal of damaged proteins and organelles, which is critical for the maintenance of energy and function homeostasis of cells. Accumulating evidence demonstrates that autophagy plays important roles in pathophysiological mechanisms under ischemic stroke. Previous investigations show that autophagy serves as a "double-edged sword" in ischemic stroke as it can either promote the survival of neuronal cells or induce cell death in special conditions. Following ischemic stroke, autophagy is activated or inhibited in several cell types in brain, including neurons, astrocytes, and microglia, as well as microvascular endothelial cells, which involves in inflammatory activation, modulation of microglial phenotypes, and blood-brain barrier permeability. However, the exact mechanisms of underlying the role of autophagy in ischemic stroke are not fully understood. This review focuses on the recent advances regarding potential molecular mechanisms of autophagy in different cell types. The focus is also on discussing the "double-edged sword" effect of autophagy in ischemic stroke and its possible underlying mechanisms. In addition, potential therapeutic strategies for ischemic stroke targeting autophagy are also reviewed.

摘要

中风是全球范围内导致死亡和残疾的主要原因之一。自噬是一种保守的细胞分解代谢途径,通过清除受损的蛋白质和细胞器来维持细胞内的平衡,这对于维持细胞的能量和功能平衡至关重要。越来越多的证据表明,自噬在缺血性中风的病理生理机制中发挥着重要作用。先前的研究表明,自噬在缺血性中风中是一把“双刃剑”,因为它既可以促进神经元细胞的存活,也可以在特殊条件下诱导细胞死亡。在缺血性中风后,包括神经元、星形胶质细胞和小胶质细胞以及微血管内皮细胞在内的几种脑细胞类型中的自噬被激活或抑制,这涉及炎症激活、小胶质细胞表型的调节和血脑屏障通透性。然而,自噬在缺血性中风中的作用的潜在机制尚不完全清楚。本综述重点介绍了自噬在不同细胞类型中潜在分子机制的最新进展。还重点讨论了自噬在缺血性中风中的“双刃剑”效应及其可能的潜在机制。此外,还综述了针对自噬的缺血性中风的潜在治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f146/9200548/07e03168a911/OMCL2022-3450207.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f146/9200548/d3fb36706aa1/OMCL2022-3450207.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f146/9200548/eb156354b0d5/OMCL2022-3450207.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f146/9200548/5a6d8f035cbe/OMCL2022-3450207.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f146/9200548/07e03168a911/OMCL2022-3450207.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f146/9200548/d3fb36706aa1/OMCL2022-3450207.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f146/9200548/eb156354b0d5/OMCL2022-3450207.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f146/9200548/5a6d8f035cbe/OMCL2022-3450207.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f146/9200548/07e03168a911/OMCL2022-3450207.004.jpg

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本文引用的文献

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2
miR-155-5p in Extracellular Vesicles Derived from Choroid Plexus Epithelial Cells Promotes Autophagy and Inflammation to Aggravate Ischemic Brain Injury in Mice.脉络丛上皮细胞来源的细胞外囊泡中的 miR-155-5p 通过促进自噬和炎症加重小鼠缺血性脑损伤。
Oxid Med Cell Longev. 2022 Feb 16;2022:8603427. doi: 10.1155/2022/8603427. eCollection 2022.
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p53 Inhibition Protects against Neuronal Ischemia/Reperfusion Injury by the p53/PRAS40/mTOR Pathway.
褪黑素通过转录因子EB上调自噬减轻酸中毒诱导的神经元损伤。
Int J Mol Sci. 2025 Jan 29;26(3):1170. doi: 10.3390/ijms26031170.
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Z-Ligustilide: A Potential Therapeutic Agent for Atherosclerosis Complicating Cerebrovascular Disease.Z-阿魏酸:一种治疗并发脑血管疾病的动脉粥样硬化的潜在治疗剂。
Biomolecules. 2024 Dec 18;14(12):1623. doi: 10.3390/biom14121623.
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