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
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
收藏
页码:863 / U1
页数:19
相关论文
共 157 条
  • [41] Phosphoproteome analysis of isoflurane-protected heart mitochondria:: phosphorylation of adenine nucleotide translocator-1 on Tyr194 regulates mitochondrial function
    Feng, Jianhua
    Zhu, Min
    Schaub, Marcus C.
    Gehrig, Peter
    Roschitzki, Bernd
    Lucchinetti, Eliana
    Zaugg, Michael
    [J]. CARDIOVASCULAR RESEARCH, 2008, 80 (01) : 20 - 29
  • [42] Interaction of cardiovascular risk factors with myocardial ischemia/reperfusion injury, preconditioning, and postconditioning
    Ferdinandy, Peter
    Schulz, Rainer
    Baxter, Gary F.
    [J]. PHARMACOLOGICAL REVIEWS, 2007, 59 (04) : 418 - 458
  • [43] SUPEROXIDE RADICAL AND SUPEROXIDE DISMUTASES
    FRIDOVICH, I
    [J]. ANNUAL REVIEW OF BIOCHEMISTRY, 1995, 64 : 97 - 112
  • [44] Isoflurane Postconditioning Protects against Reperfusion Injury by Preventing Mitochondrial Permeability Transition by an Endothelial Nitric Oxide Synthase-dependent Mechanism
    Ge, Zhi-Dong
    Pravdic, Danijel
    Bienengraeber, Martin
    Pratt, Phillip F., Jr.
    Auchampach, John A.
    Gross, Garrett J.
    Kersten, Judy R.
    Warltier, David C.
    [J]. ANESTHESIOLOGY, 2010, 112 (01) : 73 - 85
  • [45] Electron transfer between cytochrome c and p66Shc generates reactive oxygen species that trigger mitochondrial apoptosis
    Giorgio, M
    Migliaccio, E
    Orsini, F
    Paolucci, D
    Moroni, M
    Contursi, C
    Pelliccia, G
    Luzi, L
    Minucci, S
    Marcaccio, M
    Pinton, P
    Rizzuto, R
    Bernardi, P
    Paolucci, F
    Pelicci, PG
    [J]. CELL, 2005, 122 (02) : 221 - 233
  • [46] Inhibition of GSK3β by postconditioning is required to prevent opening of the mitochondrial permeability transition pore during reperfusion
    Gomez, Ludovic
    Paillard, Melanie
    Thibault, Helene
    Derumeaux, Genevieve
    Ovize, Michel
    [J]. CIRCULATION, 2008, 117 (21) : 2761 - 2768
  • [47] Cardioprotection requires taking out the trash
    Gottlieb, Roberta A.
    Finley, Kim D.
    Mentzer, Robert M., Jr.
    [J]. BASIC RESEARCH IN CARDIOLOGY, 2009, 104 (02) : 169 - 180
  • [48] Remote Postconditioning is More Potent than Classic Postconditioning in Reducing the Infarct Size in Anesthetized Rabbits
    Gritsopoulos, G.
    Iliodromitis, E. K.
    Zoga, A.
    Farmakis, D.
    Demerouti, E.
    Papalois, A.
    Paraskevaidis, I. A.
    Kremastinos, D. T.
    [J]. CARDIOVASCULAR DRUGS AND THERAPY, 2009, 23 (03) : 193 - 198
  • [49] Excessive ATP hydrolysis in ischemic myocardium by mitochondrial F1F0-ATPase: effect of selective pharmacological inhibition of mitochondrial ATPase hydrolase activity
    Grover, GJ
    Atwal, KS
    Sleph, PG
    Wang, FL
    Monshizadegan, H
    Monticello, T
    Green, DW
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2004, 287 (04): : H1747 - H1755
  • [50] GUTH BD, 1993, CIRCULATION, V87, P35