创伤性脑损伤中调节性细胞死亡的研究进展
Research Progress on Regulated Cell Death in Traumatic Brain Injury
DOI: 10.12677/jcpm.2026.51038, PDF,   
作者: 沈嵩民, 孔繁栋：济宁医学院临床医学院(附属医院)，山东 济宁；崔昌萌*：济宁医学院附属医院神经外科，山东 济宁
关键词: 创伤性脑损伤；调节性细胞死亡；凋亡；自噬；焦亡；Traumatic Brain Injury； Regulated Cell Death； Apoptosis； Autophagy； Pyroptosis
摘要: 创伤性脑损伤(TBI)是全球范围内导致死亡与致残的主要原因之一，其发病机制复杂，涉及神经细胞死亡、炎症反应、氧化应激及线粒体功能障碍等多种病理过程。近年来，随着细胞死亡研究的深入，人们逐渐认识到调节性细胞死亡(RCD)在TBI中的关键作用。RCD是一类由特定信号通路和基因调控的主动细胞死亡方式，包括凋亡、自噬、焦亡、坏死性凋亡、铁死亡和铜死亡等。这些过程既参与神经元损伤后的细胞清除，在过度激活时同时也加剧了组织炎症和神经功能障碍。本文综述了不同类型RCD在TBI发生与发展的分子机制、相互作用及其潜在治疗策略的最新研究进展，为TBI的干预和神经保护提供新的理论依据。
Abstract: Traumatic brain injury (TBI) is one of the leading causes of death and disability worldwide. Its pathogenesis is highly complex, involving multiple pathological processes such as neuronal cell death, inflammatory responses, oxidative stress, and mitochondrial dysfunction. In recent years, with advances in the study of cell death, increasing attention has been given to the critical role of regulated cell death (RCD) in TBI. RCD refers to a group of programmed cell death modalities controlled by specific signaling pathways and genetic regulation, including apoptosis, autophagy, pyroptosis, necroptosis, ferroptosis, and cuproptosis. These processes contribute to the clearance of damaged neural cells but, when excessively activated, can also exacerbate tissue inflammation and neurological dysfunction. This review summarizes the latest research progress on the molecular mechanisms, interactions, and potential therapeutic strategies of various RCD types in the occurrence and development of TBI, providing new theoretical insights for intervention and neuroprotection in TBI.
文章引用：沈嵩民, 孔繁栋, 崔昌萌. 创伤性脑损伤中调节性细胞死亡的研究进展[J]. 临床个性化医学, 2026, 5(1): 258-265. https://doi.org/10.12677/jcpm.2026.51038

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