我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

Ca2+在心肌缺血/再灌注损伤的线粒体调控机制中的作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第5期
页码:
596-599
栏目:
综述
出版日期:
2007-10-01

文章信息/Info

Title:
-
作者:
贾冰 综述臧伟进 审校
西安交通大学医学院药理学系,陕西 西安 710061
Author(s):
-
关键词:
Ca2+线粒体缺血再灌注心肌
Keywords:
-
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
线粒体作为细胞存活和死亡的主宰者发挥多种功能作用,包括氧化磷酸化作用、自由基生成以及维持细胞内Ca2+平衡。在心肌缺血过程中以及缺血后,线粒体Ca2+浓度升高、功能受损,最终导致细胞坏死或凋亡。本文主要从线粒体Ca2+浓度升高出现的原因、对线粒体功能的病理性调控作用及其诱导的自身保护机制几个方面,综述了Ca2+在心肌缺血/再灌注损伤的线粒体调控机制中的作用。
Abstract:
-

参考文献/References

[1] Kirichok Y, Krapivinsky G, Clapham DE. The mitochondrial calcium uniporter is a highly selective ion channel[J]. Nature, 2004, 427(6972):360 -364.

[2] Saotome M, Katoh H, Satoh H, et al. Mitochondrial membrane potential modulates regulation of mitochondrial Ca2+ in rat ventricular myocytes[J]. Am J Physiol Heart Circ Physiol, 2005, 288(4): H1820 -H1828.

[3] Marisol RM, David GD,Elisabet MC,et al. Mitochondrial Ca2+ uptake during simulated ischemia does not affect permeability transition pore opening upon simulated reperfusion[J]. Cardiovasc Res, 2006, 71(4): 715 -724.

[4] Chen Q, Hoppel CL, Lesnefsky EJ. Blockade of electron transport before cardiac ischemia with the reversible inhibitor amobarbital protects rat heart mitochondria[J]. J Pharmacol Exp Ther, 2006,316(1): 200 -207.

[5] Rodrigo GC,Standen NB. Role of mitochondrial reenergization and Ca2+influx in reperfusion injury of metabolically inhibited cardiac myocytes[J]. Cardiovasc Res, 2005, 67(2): 291 -300.

[6] Brookes PS, DarleyUsmar VM. Role of calcium and superoxide dismutase in sensitizing mitochondria to peroxynitriteinduced permeability transition[J]. Am J Physiol Heart Circ Physiol, 2004, 286(1): H39- H46.

[7] Argaud L, GateauRoesch O, Raisky O, et al. Postconditioning inhibits mitochondrial permeability transition[J]. Circulation, 2005, 111(2): 194 -197.

[8] Argaud L, GateauRoesch O, Muntean D, et al. Specific inhibition of the mitochondrial permeability transition prevents lethal reperfusion injury[J]. J Mol Cell Cardiol, 2005, 38(2): 367 -374.

[9 ] Bopassa JC, Michel P, GateauRoesch O, et al. Low pressure reperfusion alters mitochondrial permeability transition[J]. Am J Physiol Heart Circ Physiol, 2005, 288(6): H2750 -H2755.

[10]Tsang A, Hausenloy DJ, Yellon DM. Myocardial postconditioning: reperfusion injury revisited[J]. Am J Physiol Heart Circ Physiol, 2005, 289(1): H2-H7.

[11]赵志青,臧益民.再灌注心脏保护的新策略:后处理和预处理的比较[J].心脏杂志, 2006, 18(1):1–7,13.

[12]Kin H, Zhao ZQ, Sun HY, et al. Postconditioning attenuates myocardial ischemia reperfusion injury by inhibiting events in the early minutes of reperfusion[J]. Cardiovasc Res, 2004, 62(1): 74 -85.

[13]Nakagawa T, Shimizu S, Watanabe T, et al. Cyclophilin Ddependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death[J]. Nature, 2005, 434(7033): 652- 658.

[14]Baines CP, Kaiser RA, Purcell NH, et al. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death[J]. Nature, 2005, 434(7033): 658- 662.

[15]Halestrap A. Biochemistry:a pore way to die[J]. Nature, 2005, 434(7033): 578-579.

[16] Halestrap AP,Clarke SJ,Javadov SA.Mitochondrial permeability transition pore opening during myocardial reperfusion-a target for cardioprotection.[J].Cardiovasc Res,2004,61(3):372-385.

[17]Hausenlog DJ, Yellon DM, ManiBabu S, et al. Preconditioning protects by inhibiting the mitochondrial permeability transition[J]. Am J Physiol Heart Circ Physiol, 2004, 287(2): H841-H849.

[18]Brookes PS,Yoon Y, Robotham JL,et al. Calcium, ATP, and ROS: a mitochondrial lovehate triangle [J]. Am J Physiol Cell Physiol, 2004, 287(4): C817- C833.

[19]Basso E, Fante L, Fowlkes J, et al. Properties of the permeability transition pore in mitochondria devoid of cyclophilin D[J]. J Biol Chem, 2005, 280(19): 18558 -18561.

[20]Argaud L, GateauRoesch O, Chalabreysse L, et al. Preconditioning delays Ca2+induced mitochondrial permeability transition[J]. Cardiovasc Res, 2004,61(1): 115- 122.

[21]Brennan JP, Southworth R, Medina RA, et al. Mitochondrial uncoupling, with low concentration FCCP, induces ROSdependent cardioprotection independent of KATPchannel activation[J]. Cardiovasc Res, 2006,72(2):313-321.

[22]Iverson SL, Orrenius S. The cardiolipincytochrome c interaction and the mitochondrial regulation of apoptosis[J]. Arch Biochem Biophys, 2004, 423(1): 37–46.

[23]Sato T, Saito T, Saegusa N, et al. Mitochondrial Ca2+activated K+channels in cardiac myocytes: A mechanism of the cardioprotective effect and modulation by protein kinase A[J]. Circulation, 2005, 111(2): 198–203.

备注/Memo

备注/Memo:
收稿日期:2006-10-07.基金项目:国家重点基础研究发展计划项目资助(No.2007CB512005)通讯作者:臧伟进,教授,主要从事心血管生理药理研究 Email:zwj@mail.xjtu.edu.cn作者简介:贾 冰,博士生Email:jiabing@stu.xjtu.edu.cn
更新日期/Last Update: