Heart mitochondria:: gates of life and death

被引:328
作者
Gustafsson, Asa B. [1 ]
Gottlieb, Roberta A. [1 ]
机构
[1] San Diego State Univ, Biosci Ctr, San Diego, CA 92182 USA
关键词
apoptosis; mitochondria; myocytes; necrosis; reperfusion;
D O I
10.1093/cvr/cvm005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Mitochondria are important generators of energy, providing ATP through oxidative phosphorylation. However, mitochondria also monitor complex information from the environment and intracellular milieu, including the presence or absence of growth factors, oxygen, reactive oxygen species, and DNA damage. Mitochondria have been implicated in the loss of cells in various cardiac pathologies, including ischaemia/reperfusion injury, cardiomyopathy, and congestive heart failure. The release of factors such as cytochrome c, Smac, Omi/Htr2A, and AIF from mitochondria serves to activate a highly complex and regulated cell death program. Furthermore, mitochondrial calcium overload might trigger opening of the mitochondrial permeability transition pore, causing uncoupling of oxidative phosphorylation, swelling of the mitochondria, due to influx of water, and rupture of the mitochondrial outer membrane. In this review, we discuss the rote of mitochondria in the control of cell death in cardiac myocytes.
引用
收藏
页码:334 / 343
页数:10
相关论文
共 151 条
[1]   The Bcl-2 protein family: Arbiters of cell survival [J].
Adams, JM ;
Cory, S .
SCIENCE, 1998, 281 (5381) :1322-1326
[2]   Cardiomyocyte apoptosis induced by Gαq signaling is mediated by permeability transition pore formation and activation of the mitochondrial death pathway [J].
Adams, JW ;
Pagel, AL ;
Means, CK ;
Oksenberg, D ;
Armstrong, RC ;
Brown, JH .
CIRCULATION RESEARCH, 2000, 87 (12) :1180-1187
[3]   Enhanced Gαq signaling:: A common pathway mediates cardiac hypertrophy and apoptotic heart failure [J].
Adams, JW ;
Sakata, Y ;
Davis, MG ;
Sah, VP ;
Wang, YB ;
Liggett, SB ;
Chien, KR ;
Brown, JH ;
Dorn, GW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (17) :10140-10145
[4]   The mitochondrial origin of postischernic arrhythmias [J].
Akar, FG ;
Aon, MA ;
Tomaselli, GF ;
O'Rourke, B .
JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (12) :3527-3535
[5]   Metabolic consequences of functional complexes of mitochondria, myofibrils and sarcoplasmic reticulum in muscle cells [J].
Andrienko, T ;
Kuznetsov, AV ;
Kaambre, T ;
Usson, Y ;
Orosco, A ;
Appaix, F ;
Tiivel, T ;
Sikk, P ;
Vendelin, M ;
Margreiter, R ;
Saks, VA .
JOURNAL OF EXPERIMENTAL BIOLOGY, 2003, 206 (12) :2059-2072
[6]   Synchronized whole cell oscillations in mitochondrial metabolism triggered by a local release of reactive oxygen species in cardiac myocytes [J].
Aon, MA ;
Cortassa, S ;
Marbán, E ;
O'Rourke, B .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (45) :44735-44744
[7]   Mitochondrial KATP channels in cell survival and death [J].
Ardehali, H ;
O'Rourke, B .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2005, 39 (01) :7-16
[8]   Postconditioning inhibits mitochondrial permeability transition [J].
Argaud, L ;
Gateau-Roesch, O ;
Raisky, O ;
Loufouat, J ;
Robert, D ;
Ovize, M .
CIRCULATION, 2005, 111 (02) :194-197
[9]   Mitochondria recycle Ca2+ to the endoplasmic reticulum and prevent the depletion of neighboring endoplasmic reticulum regions [J].
Arnaudeau, S ;
Kelley, WL ;
Walsh, JV ;
Demaurex, N .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (31) :29430-29439
[10]   N-ACETYLCYSTEINE IN COMBINATION WITH NITROGLYCERIN AND STREPTOKINASE FOR THE TREATMENT OF EVOLVING ACUTE MYOCARDIAL-INFARCTION - SAFETY AND BIOCHEMICAL EFFECTS [J].
ARSTALL, MA ;
YANG, JF ;
STAFFORD, I ;
BETTS, WH ;
HOROWITZ, JD .
CIRCULATION, 1995, 92 (10) :2855-2862