Bcl-2 family members and apoptosis, taken to heart

被引:257
作者
Gustafsson, Asa B. [1 ]
Gottlieb, Roberta A. [1 ]
机构
[1] Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 2007年 / 292卷 / 01期
关键词
cardiovascular disease; cytochrome c; protein; mitochondria;
D O I
10.1152/ajpcell.00229.2006
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Loss of myocardial cells via apoptosis has been observed in many cardiovascular diseases and has been shown to contribute to the initiation and progression of heart failure. The Bcl-2 family members are important regulators of the mitochondrial pathway of apoptosis. These proteins decide whether the mitochondria should initiate the cell death program and release proapoptotic factors such as cytochrome c. The Bcl-2 proteins consist of anti- and proapoptotic members and play a key role in regulating apoptosis in the myocardium. The antiapoptotic proteins have been demonstrated to protect against various cardiac pathologies, whereas the antiapoptotic proteins have been reported to contribute to heart disease. This review summarizes the current understanding of the role of Bcl-2 proteins in the heart.
引用
收藏
页码:C45 / C51
页数:7
相关论文
共 100 条
[71]   The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex [J].
Puthalakath, H ;
Huang, DCS ;
O'Reilly, LA ;
King, SM ;
Strasser, A .
MOLECULAR CELL, 1999, 3 (03) :287-296
[72]   Inducible Expression of BNIP3 provokes mitochondrial defects and hypoxia-mediated cell death of ventricular myocytes [J].
Regula, KM ;
Ens, K ;
Kirshenbaum, LA .
CIRCULATION RESEARCH, 2002, 91 (03) :226-231
[73]   Bid, but not Bax, regulates VDAC channels [J].
Rostovtseva, TK ;
Antonsson, B ;
Suzuki, M ;
Youle, RJ ;
Colombini, M ;
Bezrukov, SM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (14) :13575-13583
[74]   EFFECTS OF OLIGOMYCIN AND ACIDOSIS ON RATES OF ATP DEPLETION IN ISCHEMIC HEART-MUSCLE [J].
ROUSLIN, W ;
ERICKSON, JL ;
SOLARO, RJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1986, 250 (03) :H503-H508
[75]  
Saraste A, 1997, CIRCULATION, V95, P320
[76]   RETRACTED: Ku70 suppresses the apoptotic translocation of Bax to mitochondria (Retracted article. See vol 9, pg 480, 2007) [J].
Sawada, M ;
Sun, WY ;
Hayes, P ;
Leskov, K ;
Boothman, DA ;
Matsuyama, S .
NATURE CELL BIOLOGY, 2003, 5 (04) :320-329
[77]   Different signaling pathways induce apoptosis in endothelial cells and cardiac myocytes during ischemia/reperfusion injury [J].
Scarabelli, TM ;
Stephanou, A ;
Pasini, E ;
Comini, L ;
Raddino, R ;
Knight, RA ;
Latchman, DS .
CIRCULATION RESEARCH, 2002, 90 (06) :745-748
[78]   MULTIPLE BCL-2 FAMILY MEMBERS DEMONSTRATE SELECTIVE DIMERIZATIONS WITH BAX [J].
SEDLAK, TW ;
OLTVAI, ZN ;
YANG, E ;
WANG, K ;
BOISE, LH ;
THOMPSON, CB ;
KORSMEYER, SJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (17) :7834-7838
[79]   Electrophysiological study of a novel large pore formed by Bax and the voltage-dependent anion channel that is permeable to cytochrome c [J].
Shimizu, S ;
Ide, T ;
Yanagida, T ;
Tsujimoto, Y .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (16) :12321-12325
[80]   Alterations in apoptotic signaling in human idiopathic cardiomyopathic hearts in failure [J].
Steenbergen, C ;
Afshari, CA ;
Petranka, JG ;
Collins, J ;
Martin, K ;
Bennett, L ;
Haugen, A ;
Bushel, P ;
Murphy, E .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2003, 284 (01) :H268-H276