• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies.创伤性脑损伤中的线粒体和线粒体靶向多潜能治疗策略。
Br J Pharmacol. 2012 Oct;167(4):699-719. doi: 10.1111/j.1476-5381.2012.02025.x.
2
Post-Injury Administration of Mitochondrial Uncouplers Increases Tissue Sparing and Improves Behavioral Outcome following Traumatic Brain Injury in Rodents.线粒体解偶联剂在损伤后给药可减少啮齿动物创伤性脑损伤后的组织损伤并改善行为结果。
J Neurotrauma. 2007 May;24(5):798-811. doi: 10.1089/neu.2006.3673.
3
Oxidative stress and mitochondrial dysfunction following traumatic brain injury: From mechanistic view to targeted therapeutic opportunities.创伤性脑损伤后的氧化应激与线粒体功能障碍:从机制视角到靶向治疗机遇
Fundam Clin Pharmacol. 2022 Aug;36(4):612-662. doi: 10.1111/fcp.12767. Epub 2022 Feb 24.
4
Traumatic brain injury and mitochondrial dysfunction.创伤性脑损伤与线粒体功能障碍
Am J Med Sci. 2015 Aug;350(2):132-8. doi: 10.1097/MAJ.0000000000000506.
5
Mitochondrial dysfunction contributes to cell death following traumatic brain injury in adult and immature animals.线粒体功能障碍导致成年和未成年动物创伤性脑损伤后的细胞死亡。
J Bioenerg Biomembr. 2004 Aug;36(4):363-8. doi: 10.1023/B:JOBB.0000041769.06954.e4.
6
Causal role of apoptosis-inducing factor for neuronal cell death following traumatic brain injury.凋亡诱导因子在创伤性脑损伤后神经元细胞死亡中的因果作用。
Am J Pathol. 2008 Dec;173(6):1795-805. doi: 10.2353/ajpath.2008.080168. Epub 2008 Nov 6.
7
The optimal dosage and window of opportunity to maintain mitochondrial homeostasis following traumatic brain injury using the uncoupler FCCP.使用解偶联剂FCCP维持创伤性脑损伤后线粒体稳态的最佳剂量和时机窗。
Exp Neurol. 2009 Aug;218(2):381-9. doi: 10.1016/j.expneurol.2009.05.023. Epub 2009 May 27.
8
Cyclosporin A attenuates acute mitochondrial dysfunction following traumatic brain injury.环孢素A可减轻创伤性脑损伤后的急性线粒体功能障碍。
Exp Neurol. 1999 Nov;160(1):226-34. doi: 10.1006/exnr.1999.7197.
9
Mitochondrial uncoupling as a therapeutic target following neuronal injury.线粒体解偶联作为神经元损伤后的治疗靶点。
J Bioenerg Biomembr. 2004 Aug;36(4):353-6. doi: 10.1023/B:JOBB.0000041767.30992.19.
10
Mitochondrial participation in ischemic and traumatic neural cell death.线粒体在缺血性和创伤性神经细胞死亡中的作用。
J Neurotrauma. 2000 Oct;17(10):843-55. doi: 10.1089/neu.2000.17.843.

引用本文的文献

1
Unlocking therapeutic potential in traumatic brain injury: exploring microenvironmental targets, signaling pathways and translational hurdles.挖掘创伤性脑损伤的治疗潜力:探索微环境靶点、信号通路及转化障碍
Inflammopharmacology. 2025 Sep;33(9):5113-5144. doi: 10.1007/s10787-025-01923-7. Epub 2025 Sep 1.
2
Temporal Changes in Mitochondria-Centric Excitotoxic Responses Following Severe Penetrating Traumatic Brain Injury.严重穿透性创伤性脑损伤后以线粒体为中心的兴奋性毒性反应的时间变化
Biomedicines. 2025 Jun 21;13(7):1520. doi: 10.3390/biomedicines13071520.
3
Fiber tract integrity in patients with brain injury and chronic health symptoms.脑损伤和慢性健康症状患者的纤维束完整性
Neuroimage Rep. 2021 Sep 13;1(4):100047. doi: 10.1016/j.ynirp.2021.100047. eCollection 2021 Dec.
4
Cellular and Molecular Interactions in CNS Injury: The Role of Immune Cells and Inflammatory Responses in Damage and Repair.中枢神经系统损伤中的细胞与分子相互作用:免疫细胞及炎症反应在损伤与修复中的作用
Cells. 2025 Jun 18;14(12):918. doi: 10.3390/cells14120918.
5
Traumatic Brain Injury and Coenzyme Q10: An Overview.创伤性脑损伤与辅酶Q10:概述
Int J Mol Sci. 2025 May 27;26(11):5126. doi: 10.3390/ijms26115126.
6
Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration.线粒体:创伤性脑损伤所致神经退行性变的隐匿引擎
Front Cell Neurosci. 2025 May 9;19:1570596. doi: 10.3389/fncel.2025.1570596. eCollection 2025.
7
Platelet Extracellular Vesicles as Natural Delivery Vehicles for Mitochondrial Dysfunction Therapy?血小板细胞外囊泡能否作为线粒体功能障碍治疗的天然递送载体?
ACS Biomater Sci Eng. 2025 May 12;11(5):2601-2621. doi: 10.1021/acsbiomaterials.5c00473. Epub 2025 Apr 25.
8
L-Carnitine and Mildronate Demonstrate Divergent Protective Effects on Mitochondrial DNA Quality Control and Inflammation Following Traumatic Brain Injury.左旋肉碱和米屈肼对创伤性脑损伤后的线粒体DNA质量控制和炎症表现出不同的保护作用。
Int J Mol Sci. 2025 Mar 22;26(7):2902. doi: 10.3390/ijms26072902.
9
Concussion injuries in sports and the role of instrumented mouthguards: a mini review.运动中的脑震荡损伤与智能护齿器的作用:一篇综述短文
Front Bioeng Biotechnol. 2025 Apr 1;13:1567429. doi: 10.3389/fbioe.2025.1567429. eCollection 2025.
10
Unraveling cell death mechanisms in traumatic brain injury: dynamic roles of ferroptosis and necroptosis.揭示创伤性脑损伤中的细胞死亡机制:铁死亡和坏死性凋亡的动态作用
Mol Biol Rep. 2025 Apr 10;52(1):381. doi: 10.1007/s11033-025-10489-0.

本文引用的文献

1
Hypothermia for acute brain injury--mechanisms and practical aspects.急性脑损伤的低温治疗——机制与实际问题。
Nat Rev Neurol. 2012 Feb 28;8(4):214-22. doi: 10.1038/nrneurol.2012.21.
2
Post-injury administration of the mitochondrial permeability transition pore inhibitor, NIM811, is neuroprotective and improves cognition after traumatic brain injury in rats.创伤性脑损伤后给予线粒体通透性转换孔抑制剂 NIM811 具有神经保护作用并改善认知功能。
J Neurotrauma. 2011 Sep;28(9):1845-53. doi: 10.1089/neu.2011.1755. Epub 2011 Aug 29.
3
Distinctive characteristics and functions of multiple mitochondrial Ca2+ influx mechanisms.多种线粒体 Ca2+内流机制的独特特征和功能。
Sci China Life Sci. 2011 Aug;54(8):763-9. doi: 10.1007/s11427-011-4203-9. Epub 2011 Jul 24.
4
Brain energy depletion in a rodent model of diffuse traumatic brain injury is not prevented with administration of sodium lactate.在弥漫性创伤性脑损伤的啮齿动物模型中,给予乳酸钠不能防止脑能量耗竭。
Brain Res. 2011 Aug 2;1404:39-49. doi: 10.1016/j.brainres.2011.06.006. Epub 2011 Jun 12.
5
Mitochondrial permeability transition in Ca(2+)-dependent apoptosis and necrosis.钙离子依赖型细胞凋亡和坏死中的线粒体通透性转换。
Cell Calcium. 2011 Sep;50(3):222-33. doi: 10.1016/j.ceca.2011.04.007. Epub 2011 May 23.
6
The roles of phosphate and the phosphate carrier in the mitochondrial permeability transition pore.磷酸盐和磷酸盐载体在线粒体通透性转换孔中的作用。
Mitochondrion. 2012 Jan;12(1):120-5. doi: 10.1016/j.mito.2011.04.006. Epub 2011 May 8.
7
Plasma membrane calcium pump regulation by metabolic stress.代谢应激对质膜钙泵的调节
World J Biol Chem. 2010 Jul 26;1(7):221-8. doi: 10.4331/wjbc.v1.i7.221.
8
Broad-spectrum neuroprotection against traumatic brain injury by agonism of peroxisome proliferator-activated receptors.激动过氧化物酶体增殖物激活受体对创伤性脑损伤的广谱神经保护作用。
Exp Neurol. 2011 Jun;229(2):195-7. doi: 10.1016/j.expneurol.2011.02.002. Epub 2011 Feb 21.
9
Bcl-2 proteins and mitochondria--specificity in membrane targeting for death.Bcl-2蛋白与线粒体——死亡相关膜靶向的特异性
Biochim Biophys Acta. 2011 Apr;1813(4):532-9. doi: 10.1016/j.bbamcr.2010.10.017. Epub 2010 Nov 5.
10
Modes of Neuronal Calcium Entry and Homeostasis following Cerebral Ischemia.脑缺血后神经元钙内流及钙稳态的模式
Stroke Res Treat. 2010 Nov 1;2010:316862. doi: 10.4061/2010/316862.

创伤性脑损伤中的线粒体和线粒体靶向多潜能治疗策略。

Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies.

机构信息

Neurosurgical Department, PLA Navy General Hospital, Beijing, China.

出版信息

Br J Pharmacol. 2012 Oct;167(4):699-719. doi: 10.1111/j.1476-5381.2012.02025.x.

DOI:10.1111/j.1476-5381.2012.02025.x
PMID:23003569
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3575772/
Abstract

Traumatic brain injury (TBI) is a major health and socioeconomic problem throughout the world. It is a complicated pathological process that consists of primary insults and a secondary insult characterized by a set of biochemical cascades. The imbalance between a higher energy demand for repair of cell damage and decreased energy production led by mitochondrial dysfunction aggravates cell damage. At the cellular level, the main cause of the secondary deleterious cascades is cell damage that is centred in the mitochondria. Excitotoxicity, Ca(2+) overload, reactive oxygen species (ROS), Bcl-2 family, caspases and apoptosis inducing factor (AIF) are the main participants in mitochondria-centred cell damage following TBI. Some preclinical and clinical results of mitochondria-targeted therapy show promise. Mitochondria- targeted multipotential therapeutic strategies offer new hope for the successful treatment of TBI and other acute brain injuries.

摘要

创伤性脑损伤(TBI)是全球范围内的一个主要健康和社会经济问题。它是一个复杂的病理过程,由原发性损伤和以一系列生化级联反应为特征的继发性损伤组成。线粒体功能障碍导致的细胞损伤修复的高能量需求与能量产生减少之间的失衡,加剧了细胞损伤。在细胞水平上,继发性有害级联反应的主要原因是集中在线粒体的细胞损伤。兴奋性毒性、Ca(2+)超载、活性氧(ROS)、Bcl-2 家族、半胱天冬酶和凋亡诱导因子(AIF)是 TBI 后以线粒体为中心的细胞损伤的主要参与者。一些针对线粒体的治疗的临床前和临床结果显示出希望。针对线粒体的多潜能治疗策略为成功治疗 TBI 和其他急性脑损伤提供了新的希望。