Mitochondria in Postconditioning

被引：51

作者：

Boengler, Kerstin ^{[1
]}

Heusch, Gerd ^{[1
]}

Schulz, Rainer ^{[1
]}

机构：

[1] Univ Klinikum Essen, Zentrum Innere Med, Inst Pathophysiol, D-45122 Essen, Germany

来源：

ANTIOXIDANTS & REDOX SIGNALING | 2011年 / 14卷 / 05期

关键词：

PERMEABILITY TRANSITION PORE; ISCHEMIA-REPERFUSION INJURY; K-ATP CHANNELS; GLYCOGEN-SYNTHASE KINASE-3-BETA; MYOCARDIAL INFARCT SIZE; BRIEF RENAL ISCHEMIA; ISOLATED RAT HEARTS; REACTIVE OXYGEN; FREE-RADICALS; SIGNALING PATHWAYS;

D O I：

10.1089/ars.2010.3309

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Several signal transduction pathways are activated by cardioprotective stimuli, including ischemic or pharmacological postconditioning. These pathways converge on a common target, the mitochondria, and cardioprotection by postconditioning is associated with preserved mitochondrial function after ischemia/reperfusion. The present review discusses the role of mitochondria in cardioprotection, especially the involvement of ATP-dependent potassium channels, reactive oxygen species, and the mitochondrial permeability transition pore, and focuses on the effects of postconditioning on mitochondrial function (i.e., their oxygen consumption and calcium retention capacity). The contribution of mitochondria to loss of protection by postconditioning in diseased or aged myocardium is also addressed. Antioxid. Redox Signal. 14, 863-880.

引用

页码：863 / U1

页数：19

共 157 条

[1] Ischemic threshold and myocardial stunning in the aging heart
Abete, P
Cioppa, A
Calabrese, C
Pascucci, I
Cacciatore, F
Napoli, C
Carnovale, V
Ferrara, N
Rengo, F
[J]. EXPERIMENTAL GERONTOLOGY, 1999, 34 (07) : 875 - 884
[2] Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury
Adlam, VJ
Harrison, JC
Porteous, CM
James, AM
Smith, RAJ
Murphy, MP
Sammut, IA
[J]. FASEB JOURNAL, 2005, 19 (09) : 1088 - 1095
[3] NADPH oxidase signaling and cardiac myocyte function
Akki, Ashwin
Zhang, Min
Murdoch, Colin
Brewer, Alison
Shah, Ajay M.
[J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2009, 47 (01) : 15 - 22
[4] Opening mitoKATP increases superoxide generation from complex I of the electron transport chain
Andrukhiv, Anastasia
Costa, Alexandre D.
West, Ian C.
Garlid, Keith D.
[J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2006, 291 (05): : H2067 - H2074
[5] Mitochondrial KATP channels in cell survival and death
Ardehali, H
O'Rourke, B
[J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2005, 39 (01) : 7 - 16
[6] Postconditioning inhibits mitochondrial permeability transition
Argaud, L
Gateau-Roesch, O
Raisky, O
Loufouat, J
Robert, D
Ovize, M
[J]. CIRCULATION, 2005, 111 (02) : 194 - 197
[7] Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts
Argaud, Laurent
Gateau-Roesch, Odile
Augeul, Lionel
Couture-Lepetit, Elisabeth
Loufouat, Joseph
Gomez, Ludovic
Robert, Dominique
Ovize, Michel
[J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2008, 294 (01): : H386 - H391
[8] Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death
Baines, Christopher P.
Kaiser, Robert A.
Sheiko, Tatiana
Craigen, William J.
Molkentin, Jeffery D.
[J]. NATURE CELL BIOLOGY, 2007, 9 (05) : 550 - U122
[9] Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
Baines, CP
Kaiser, RA
Purcell, NH
Blair, NS
Osinska, H
Hambleton, MA
Brunskill, EW
Sayen, MR
Gottlieb, RA
Dorn, GW
Robbins, J
Molkentin, JD
[J]. NATURE, 2005, 434 (7033) : 658 - 662
[10] Oxygen radicals released during ischemic preconditioning contribute to cardioprotection in the rabbit myocardium
Baines, CP
Goto, M
Downey, JM
[J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1997, 29 (01) : 207 - 216

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