异丙酚诱导的压电通道术后认知功能障碍研究进展。

IF 3.8 3区 医学 Q2 NEUROSCIENCES
Frontiers in Molecular Neuroscience Pub Date : 2025-09-22 eCollection Date: 2025-01-01 DOI:10.3389/fnmol.2025.1668523
Han Xue, Xiaoyu Zhang, Chenxu Chou, Yulong Jia, Chunguang Hao, Xiaguang Duan
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引用次数: 0

摘要

术后认知功能障碍(POCD)常发生在麻醉和手术后的老年患者身上,其特征是记忆丧失、注意力不集中、思维和决策困难。异丙酚是一种常用的静脉麻醉剂。它对大脑的影响是复杂的,研究人员一直在密切关注这些影响。虽然它在某些情况下可以保护神经细胞,但它也可能造成损伤。新出现的证据表明,机械敏感的压电离子通道可能是关键的介质。这些通道允许细胞检测机械力并将其转化为生物信号。它们可能是异丙酚使用和认知能力下降之间的联系。这篇综述强调了异丙酚如何影响压电通道功能的新发现。这表明异丙酚改变了细胞膜的物理性质。它使细胞膜更硬,流动性更少。这些变化可能会改变压电通道对机械力的反应。它们会干扰大脑中的钙信号和突触功能。这个问题会增加炎症和对线粒体的损害。它会削弱突触连接,导致认知能力下降,尤其是在老年人中。此外,钙通过Piezo1通道进入与炎症有关,这可能是异丙酚和压电通道共同导致POCD的另一种机制。然而,关于异丙酚如何与压电通道相互作用的明确证据仍然缺乏。需要更多的分子模拟、遗传模型和钙成像研究来更好地理解这些过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Advances in research on propofol-induced postoperative cognitive dysfunction via Piezo channels.

Postoperative cognitive dysfunction (POCD), which often affects elderly patients after anesthesia and surgery, is characterized by memory loss, trouble concentrating, and difficulties with thinking and decision-making. Propofol is a commonly used intravenous anesthetic. Its effects on the brain are complex, and researchers have been paying closer attention to them. While it can protect nerve cells in some situations, it may also cause damage. Emerging evidence suggests that mechanosensitive Piezo ion channels may serve as critical mediators. These channels allow cells to detect mechanical forces and turn them into biological signals. They may act as a link between propofol use and cognitive decline. This review highlights new findings on how propofol may affect Piezo channel function. It shows that propofol changes the physical properties of cell membranes. It makes the membranes stiffer and less fluid. These changes may change how Piezo channels react to mechanical forces. They can disturb calcium signals and synaptic function in the brain. This problem can increase inflammation and damage to mitochondria. It can weaken synaptic connections and cause cognitive decline, especially in older adults. Additionally, calcium entering through Piezo1 channels has been linked to inflammation, which may be another mechanism by which propofol and Piezo channels together cause POCD. However, clear proof of how propofol interacts with Piezo channels is still lacking. More research with molecular simulations, genetic models, and calcium imaging is needed to better understand these processes.

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来源期刊
CiteScore
5.70
自引率
2.10%
发文量
669
审稿时长
14 weeks
期刊介绍: Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.
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