• 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
The molecular composition of the mitochondrial permeability transition pore.线粒体通透性转换孔的分子组成。
J Mol Cell Cardiol. 2009 Jun;46(6):850-7. doi: 10.1016/j.yjmcc.2009.02.007. Epub 2009 Feb 20.
2
Role of the c subunit of the FO ATP synthase in mitochondrial permeability transition.FO ATP 合酶 C 亚基在线粒体通透性转换中的作用。
Cell Cycle. 2013 Feb 15;12(4):674-83. doi: 10.4161/cc.23599. Epub 2013 Jan 23.
3
Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death.电压依赖性阴离子通道对于线粒体依赖性细胞死亡是可有可无的。
Nat Cell Biol. 2007 May;9(5):550-5. doi: 10.1038/ncb1575. Epub 2007 Apr 8.
4
The permeability transition pore in cell death.细胞死亡中的通透性转换孔
Apoptosis. 2007 May;12(5):841-55. doi: 10.1007/s10495-007-0747-3.
5
Role of the mitochondrial membrane permeability transition in cell death.线粒体膜通透性转换在细胞死亡中的作用。
Apoptosis. 2007 May;12(5):835-40. doi: 10.1007/s10495-006-0525-7.
6
The mitochondrial permeability transition pore and ischemia-reperfusion injury.线粒体通透性转换孔与缺血再灌注损伤
Basic Res Cardiol. 2009 Mar;104(2):181-8. doi: 10.1007/s00395-009-0004-8. Epub 2009 Feb 26.
7
The mitochondrial permeability transition pore: Is it formed by the ATP synthase, adenine nucleotide translocators or both?线粒体通透性转换孔:它是由ATP合酶、腺嘌呤核苷酸转运体还是两者共同形成的?
Biochim Biophys Acta Bioenerg. 2020 Oct 1;1861(10):148249. doi: 10.1016/j.bbabio.2020.148249. Epub 2020 Jun 20.
8
Not all mitochondrial carrier proteins support permeability transition pore formation: no involvement of uncoupling protein 1.并非所有的线粒体载体蛋白都支持通透性转换孔的形成:解偶联蛋白 1 不参与其中。
Biosci Rep. 2009 Dec 15;30(3):187-92. doi: 10.1042/BSR20090063.
9
Mitochondrial apoptosis without VDAC.无电压依赖性阴离子通道的线粒体凋亡
Nat Cell Biol. 2007 May;9(5):487-9. doi: 10.1038/ncb0507-487.
10
Glycogen synthase kinase 3 inhibition slows mitochondrial adenine nucleotide transport and regulates voltage-dependent anion channel phosphorylation.糖原合酶激酶3抑制作用减缓线粒体腺嘌呤核苷酸转运并调节电压依赖性阴离子通道磷酸化。
Circ Res. 2008 Oct 24;103(9):983-91. doi: 10.1161/CIRCRESAHA.108.178970. Epub 2008 Sep 18.

引用本文的文献

1
The neuroimmune nexus: unraveling the role of the mtDNA-cGAS-STING signal pathway in Alzheimer's disease.神经免疫联系:揭示线粒体DNA-环鸟苷酸-腺苷酸合成酶-干扰素基因刺激蛋白信号通路在阿尔茨海默病中的作用
Mol Neurodegener. 2025 Mar 4;20(1):25. doi: 10.1186/s13024-025-00815-2.
2
A pathogenic mutation in the ALS/FTD gene VCP induces mitochondrial hypermetabolism by modulating the permeability transition pore.ALS/FTD 基因 VCP 的致病性突变通过调节通透性转换孔诱导线粒体过度代谢。
Acta Neuropathol Commun. 2024 Oct 10;12(1):161. doi: 10.1186/s40478-024-01866-0.
3
Kidney Intrinsic Mechanisms as Novel Targets in Renovascular Hypertension.肾脏内在机制在肾血管性高血压中的新靶点作用
Hypertension. 2024 Feb;81(2):206-217. doi: 10.1161/HYPERTENSIONAHA.123.21362. Epub 2023 Oct 23.
4
Mitochondrial dysfunction at the crossroad of cardiovascular diseases and cancer.线粒体功能障碍:心血管疾病与癌症的交汇点
J Transl Med. 2023 Sep 19;21(1):635. doi: 10.1186/s12967-023-04498-5.
5
Lucialdehyde B suppresses proliferation and induces mitochondria-dependent apoptosis in nasopharyngeal carcinoma CNE2 cells.吕西亚醛 B 抑制鼻咽癌细胞 CNE2 的增殖并诱导其线粒体依赖性凋亡。
Pharm Biol. 2023 Dec;61(1):918-926. doi: 10.1080/13880209.2023.2220754.
6
Minimizing Ischemia Reperfusion Injury in Xenotransplantation.最小化异种移植中的缺血再灌注损伤。
Front Immunol. 2021 Sep 9;12:681504. doi: 10.3389/fimmu.2021.681504. eCollection 2021.
7
Mitochondrial Permeability Transition: A Pore Intertwines Brain Aging and Alzheimer's Disease.线粒体通透性转换:一个孔交织着大脑衰老和阿尔茨海默病。
Cells. 2021 Mar 15;10(3):649. doi: 10.3390/cells10030649.
8
HSP27 role in cardioprotection by modulating chemotherapeutic doxorubicin-induced cell death.热休克蛋白 27 通过调节化疗药物阿霉素诱导的细胞死亡在心脏保护中的作用。
J Mol Med (Berl). 2021 Jun;99(6):771-784. doi: 10.1007/s00109-021-02048-4. Epub 2021 Mar 16.
9
Chronic Intermittent Mild Whole-Body Hypothermia Is Therapeutic in a Mouse Model of ALS.慢性间歇性轻度全身低温对 ALS 小鼠模型具有治疗作用。
Cells. 2021 Feb 4;10(2):320. doi: 10.3390/cells10020320.
10
Physiological Ca Transients Versus Pathological Steady-State Ca Elevation, Who Flips the ROS Coin in Skeletal Muscle Mitochondria.生理性钙瞬变与病理性稳态钙升高,谁在骨骼肌线粒体中翻转活性氧这枚硬币。
Front Physiol. 2020 Oct 22;11:595800. doi: 10.3389/fphys.2020.595800. eCollection 2020.

本文引用的文献

1
Adenine nucleotide translocase-1 induces cardiomyocyte death through upregulation of the pro-apoptotic protein Bax.腺嘌呤核苷酸转位酶-1通过上调促凋亡蛋白Bax诱导心肌细胞死亡。
J Mol Cell Cardiol. 2009 Jun;46(6):969-77. doi: 10.1016/j.yjmcc.2009.01.016.
2
Increased expression and intramitochondrial translocation of cyclophilin-D associates with increased vulnerability of the permeability transition pore to stress-induced opening during compensated ventricular hypertrophy.亲环蛋白-D的表达增加及线粒体内易位与代偿性心室肥大期间通透性转换孔对压力诱导开放的易感性增加相关。
J Mol Cell Cardiol. 2009 Mar;46(3):420-30. doi: 10.1016/j.yjmcc.2008.10.020. Epub 2008 Nov 6.
3
Respiratory complex I dysfunction due to mitochondrial DNA mutations shifts the voltage threshold for opening of the permeability transition pore toward resting levels.线粒体DNA突变导致的呼吸链复合体I功能障碍使通透性转换孔开放的电压阈值向静息水平偏移。
J Biol Chem. 2009 Jan 23;284(4):2045-52. doi: 10.1074/jbc.M807321200. Epub 2008 Dec 1.
4
Myocardial overexpression of adenine nucleotide translocase 1 ameliorates diabetic cardiomyopathy in mice.腺嘌呤核苷酸转位酶1在心肌中的过表达可改善小鼠糖尿病性心肌病。
Exp Physiol. 2009 Feb;94(2):220-7. doi: 10.1113/expphysiol.2008.044800. Epub 2008 Oct 22.
5
Effect of cyclosporine on reperfusion injury in acute myocardial infarction.环孢素对急性心肌梗死再灌注损伤的影响。
N Engl J Med. 2008 Jul 31;359(5):473-81. doi: 10.1056/NEJMoa071142.
6
The mitochondrial phosphate carrier interacts with cyclophilin D and may play a key role in the permeability transition.线粒体磷酸盐载体与亲环蛋白D相互作用,可能在通透性转换中起关键作用。
J Biol Chem. 2008 Sep 26;283(39):26312-23. doi: 10.1074/jbc.M805235200. Epub 2008 Jul 30.
7
Investigation of Debio 025, a cyclophilin inhibitor, in the dystrophic mdx mouse, a model for Duchenne muscular dystrophy.亲环素抑制剂Debio 025在杜氏肌营养不良症模型——营养不良性mdx小鼠中的研究。
Br J Pharmacol. 2008 Oct;155(4):574-84. doi: 10.1038/bjp.2008.285. Epub 2008 Jul 21.
8
Over-expression of adenine nucleotide translocase 1 (ANT1) induces apoptosis and tumor regression in vivo.腺嘌呤核苷酸转位酶1(ANT1)的过表达在体内诱导细胞凋亡和肿瘤消退。
BMC Cancer. 2008 Jun 4;8:160. doi: 10.1186/1471-2407-8-160.
9
MITOCHIP assessment of differential gene expression in the skeletal muscle of Ant1 knockout mice: coordinate regulation of OXPHOS, antioxidant, and apoptotic genes.Ant1基因敲除小鼠骨骼肌中差异基因表达的线粒体芯片评估:氧化磷酸化、抗氧化和凋亡基因的协同调控
Biochim Biophys Acta. 2008 Jul-Aug;1777(7-8):666-75. doi: 10.1016/j.bbabio.2008.03.015. Epub 2008 Mar 28.
10
Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury.急性心脏缺血再灌注损伤的保护机制。
Physiol Rev. 2008 Apr;88(2):581-609. doi: 10.1152/physrev.00024.2007.

线粒体通透性转换孔的分子组成。

The molecular composition of the mitochondrial permeability transition pore.

作者信息

Baines Christopher P

机构信息

Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, Missouri 65211, USA.

出版信息

J Mol Cell Cardiol. 2009 Jun;46(6):850-7. doi: 10.1016/j.yjmcc.2009.02.007. Epub 2009 Feb 20.

DOI:10.1016/j.yjmcc.2009.02.007
PMID:19233198
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2683186/
Abstract

Uncontrolled cell death is a fundamental cause of organ disease in humans. However, despite the need for us to delineate the molecular machinery that underlies cardiomyocyte death, our knowledge of these lethal cellular processes is still limited. The discovery that mitochondrial dysfunction, and in particular the mitochondrial permeability transition (MPT) pore, is often a common cause of the cardiac cell mortality that underlies numerous cardiac diseases has been a first crucial step. The purpose of this review is to outline our current understanding of the molecular identity of the MPT pore and the many questions that still need to be answered.

摘要

不受控制的细胞死亡是人类器官疾病的一个根本原因。然而,尽管我们需要描绘出心肌细胞死亡背后的分子机制,但我们对这些致命细胞过程的了解仍然有限。线粒体功能障碍,尤其是线粒体通透性转换(MPT)孔,往往是众多心脏疾病所导致的心肌细胞死亡的常见原因,这一发现是关键的第一步。本综述的目的是概述我们目前对MPT孔分子特性的理解以及仍需解答的诸多问题。