{"title":"异丙酚诱导的压电通道术后认知功能障碍研究进展。","authors":"Han Xue, Xiaoyu Zhang, Chenxu Chou, Yulong Jia, Chunguang Hao, Xiaguang Duan","doi":"10.3389/fnmol.2025.1668523","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"18 ","pages":"1668523"},"PeriodicalIF":3.8000,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12497585/pdf/","citationCount":"0","resultStr":"{\"title\":\"Advances in research on propofol-induced postoperative cognitive dysfunction via Piezo channels.\",\"authors\":\"Han Xue, Xiaoyu Zhang, Chenxu Chou, Yulong Jia, Chunguang Hao, Xiaguang Duan\",\"doi\":\"10.3389/fnmol.2025.1668523\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":12630,\"journal\":{\"name\":\"Frontiers in Molecular Neuroscience\",\"volume\":\"18 \",\"pages\":\"1668523\"},\"PeriodicalIF\":3.8000,\"publicationDate\":\"2025-09-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12497585/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Frontiers in Molecular Neuroscience\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3389/fnmol.2025.1668523\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Molecular Neuroscience","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3389/fnmol.2025.1668523","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
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.
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.