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细胞外囊泡:围手术期医学、重症监护和疼痛管理中细胞通讯的新模式。

Extracellular Vesicles: A New Paradigm for Cellular Communication in Perioperative Medicine, Critical Care, and Pain Management.

机构信息

From the Veterans Administration San Diego Healthcare System, Department of Anesthesiology, San Diego, California.

Department of Anesthesiology, University of California, San Diego School of Medicine, San Diego, California.

出版信息

Anesth Analg. 2021 Nov 1;133(5):1162-1179. doi: 10.1213/ANE.0000000000005655.

DOI:10.1213/ANE.0000000000005655
PMID:34304233
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8542619/
Abstract

Extracellular vesicles (EVs) play critical roles in many health and disease states, including ischemia, inflammation, and pain, which are major concerns in the perioperative period and in critically ill patients. EVs are functionally active, nanometer-sized, membrane-bound vesicles actively secreted by all cells. Cell signaling is essential to physiological and pathological processes, and EVs have recently emerged as key players in intercellular communication. Recent studies in EV biology have improved our mechanistic knowledge of the pathophysiological processes in perioperative and critical care patients. Studies also show promise in using EVs in novel diagnostic and therapeutic clinical applications. This review considers the current advances and gaps in knowledge of EVs in the areas of ischemia, inflammation, pain, and in organ systems that are most relevant to anesthesiology, perioperative medicine, critical care, and pain management. We expect the reader will better understand the relationship between EVs and perioperative and critical care pathophysiological states and their potential use as novel diagnostic and therapeutic modalities.

摘要

细胞外囊泡(EVs)在许多健康和疾病状态中发挥着关键作用,包括缺血、炎症和疼痛,这些都是围手术期和重症患者的主要关注点。EVs 是具有功能活性的、纳米级大小的、由所有细胞主动分泌的膜结合囊泡。细胞信号转导对于生理和病理过程至关重要,而 EVs 最近已成为细胞间通讯的关键参与者。EV 生物学的最新研究提高了我们对围手术期和重症患者病理生理过程的机制认识。研究还表明,在新型诊断和治疗临床应用中使用 EV 具有广阔的前景。本综述考虑了在缺血、炎症、疼痛以及与麻醉学、围手术期医学、重症监护和疼痛管理最相关的器官系统中 EV 领域的最新进展和知识空白。我们期望读者能够更好地理解 EVs 与围手术期和重症患者病理生理状态之间的关系,以及它们作为新型诊断和治疗方式的潜在用途。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0e/8542619/48acdc31d819/nihms-1709572-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0e/8542619/72f1cbec5556/nihms-1709572-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0e/8542619/48acdc31d819/nihms-1709572-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0e/8542619/72f1cbec5556/nihms-1709572-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0e/8542619/48acdc31d819/nihms-1709572-f0002.jpg

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本文引用的文献

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Exosomes from neuronal stem cells may protect the heart from ischaemia/reperfusion injury via JAK1/2 and gp130.神经元干细胞来源的外泌体可通过 JAK1/2 和 gp130 保护心脏免受缺血/再灌注损伤。
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Bone marrow mesenchymal stem cell-derived exosomes attenuate cerebral ischemia-reperfusion injury-induced neuroinflammation and pyroptosis by modulating microglia M1/M2 phenotypes.骨髓间充质干细胞来源的外泌体通过调节小胶质细胞 M1/M2 表型减轻脑缺血再灌注损伤引起的神经炎症和焦亡。
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Exosomal LINC00174 derived from vascular endothelial cells attenuates myocardial I/R injury via p53-mediated autophagy and apoptosis.
源自血管内皮细胞的外泌体LINC00174通过p53介导的自噬和凋亡减轻心肌缺血/再灌注损伤。
Mol Ther Nucleic Acids. 2021 Feb 10;23:1304-1322. doi: 10.1016/j.omtn.2021.02.005. eCollection 2021 Mar 5.
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Myocardial ischemia-reperfusion induced cardiac extracellular vesicles harbour proinflammatory features and aggravate heart injury.心肌缺血再灌注诱导的心脏细胞外囊泡具有促炎特征,加重心脏损伤。
J Extracell Vesicles. 2021 Feb;10(4):e12072. doi: 10.1002/jev2.12072. Epub 2021 Feb 23.
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Engineering extracellular vesicles with platelet membranes fusion enhanced targeted therapeutic angiogenesis in a mouse model of myocardial ischemia reperfusion.利用血小板膜融合工程化细胞外囊泡增强心肌缺血再灌注小鼠模型中的靶向治疗性血管生成。
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MircoRNA-29a in Astrocyte-derived Extracellular Vesicles Suppresses Brain Ischemia Reperfusion Injury via TP53INP1 and the NF-κB/NLRP3 Axis.星形细胞来源的细胞外囊泡中的 microRNA-29a 通过 TP53INP1 和 NF-κB/NLRP3 轴抑制脑缺血再灌注损伤。
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Extracellular vesicles from anoxia preconditioned mesenchymal stem cells alleviate myocardial ischemia/reperfusion injury.缺氧预处理间充质干细胞来源的细胞外囊泡减轻心肌缺血/再灌注损伤。
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Exosomal microRNA-22-3p alleviates cerebral ischemic injury by modulating KDM6B/BMP2/BMF axis.外泌体 microRNA-22-3p 通过调节 KDM6B/BMP2/BMF 轴缓解脑缺血损伤。
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