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揭示隐藏的危险:麻醉诱导发育性神经毒性中非细胞凋亡程序性细胞死亡的综述。

Unveiling the hidden dangers: a review of non-apoptotic programmed cell death in anesthetic-induced developmental neurotoxicity.

机构信息

Translational Medical Innovation Center, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, Jiangsu, China.

Department of Anesthesiology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, Jiangsu, China.

出版信息

Cell Biol Toxicol. 2024 Aug 2;40(1):63. doi: 10.1007/s10565-024-09895-0.

DOI:10.1007/s10565-024-09895-0
PMID:39093513
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11297112/
Abstract

Anesthetic-induced developmental neurotoxicity (AIDN) can arise due to various factors, among which aberrant nerve cell death is a prominent risk factor. Animal studies have reported that repeated or prolonged anesthetic exposure can cause significant neuroapoptosis in the developing brain. Lately, non-apoptotic programmed cell deaths (PCDs), characterized by inflammation and oxidative stress, have gained increasing attention. Substantial evidence suggests that non-apoptotic PCDs are essential for neuronal cell death in AIDN compared to apoptosis. This article examines relevant publications in the PubMed database until April 2024. Only original articles in English that investigated the potential manifestations of non-apoptotic PCD in AIDN were analysed. Specifically, it investigates necroptosis, pyroptosis, ferroptosis, and parthanatos, elucidating the signaling mechanisms associated with each form. Furthermore, this study explores the potential relevance of these non-apoptotic PCDs pathways to the pathological mechanisms underlying AIDN, drawing upon their distinctive characteristics. Despite the considerable challenges involved in translating fundamental scientific knowledge into clinical therapeutic interventions, this comprehensive review offers a theoretical foundation for developing innovative preventive and treatment strategies targeting non-apoptotic PCDs in the context of AIDN.

摘要

麻醉诱导的发育性神经毒性(AIDN)可能由多种因素引起,其中异常的神经细胞死亡是一个突出的风险因素。动物研究报告称,反复或长时间暴露于麻醉剂会导致发育中的大脑发生显著的神经细胞凋亡。最近,非凋亡程序性细胞死亡(PCD),其特征为炎症和氧化应激,引起了越来越多的关注。大量证据表明,与凋亡相比,非凋亡 PCD 对于 AIDN 中的神经元细胞死亡是必不可少的。本文对截至 2024 年 4 月的 PubMed 数据库中的相关出版物进行了审查。仅分析了以英语发表的、研究 AIDN 中非凋亡 PCD 潜在表现的原创文章。具体而言,本文研究了坏死性凋亡、细胞焦亡、铁死亡和 Parthanatos,阐明了与每种形式相关的信号机制。此外,本研究还探讨了这些非凋亡 PCD 途径与 AIDN 病理机制的潜在相关性,利用它们的独特特征。尽管将基础科学知识转化为临床治疗干预存在相当大的挑战,但本综述为开发针对 AIDN 中非凋亡 PCD 的创新预防和治疗策略提供了理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecb7/11297112/2f6c28db0403/10565_2024_9895_Fig5_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecb7/11297112/723faa1ff706/10565_2024_9895_Fig2_HTML.jpg
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本文引用的文献

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Epigenetic Mechanism of SETD1B-mediated Histone Methylation in Cognitive Impairment Induced by Sevoflurane Anesthesia in Neonatal Mice.SETD1B 介导的组蛋白甲基化在七氟醚麻醉诱导新生小鼠认知障碍中的表观遗传机制。
Neuroscience. 2024 May 3;545:1-15. doi: 10.1016/j.neuroscience.2024.02.005. Epub 2024 Mar 4.
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Repeated Ketamine Anesthesia during the Neonatal Period Impairs Hippocampal Neurogenesis and Long-Term Neurocognitive Function by Inhibiting Mfn2-Mediated Mitochondrial Fusion in Neural Stem Cells.反复新生期氯胺酮麻醉通过抑制神经干细胞中 Mfn2 介导的线粒体融合来损害海马神经发生和长期神经认知功能。
Mol Neurobiol. 2024 Aug;61(8):5459-5480. doi: 10.1007/s12035-024-03921-2. Epub 2024 Jan 10.
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The microRNA-211-5p/P2RX7/ERK/GPX4 axis regulates epilepsy-associated neuronal ferroptosis and oxidative stress.
微小 RNA-211-5p/P2RX7/ERK/GPX4 轴调控癫痫相关神经元铁死亡和氧化应激。
J Neuroinflammation. 2024 Jan 8;21(1):13. doi: 10.1186/s12974-023-03009-z.
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Curcumin-ZnO conjugated nanoparticles confer neuroprotection against ketamine-induced neurotoxicity.姜黄素-ZnO 缀合纳米粒子对氯胺酮诱导的神经毒性具有神经保护作用。
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