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

页码：C45 / C51

页数：7

共 100 条

[21] BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis [J].

Danial, NN ;

Gramm, CF ;

Scorrano, L ;

Zhang, CY ;

Krauss, S ;

Ranger, AM ;

Datta, SR ;

Greenberg, ME ;

Licklider, LJ ;

Lowell, BB ;

Gygi, SP ;

Korsmeyer, SJ .

NATURE, 2003, 424 (6951) :952-956

[22] Left ventricular wall stress as a direct correlate of cardiomyocyte apoptosis in patients with severe dilated cardiomyopathy [J].

Di Napoli, P ;

Taccardi, AA ;

Grilli, A ;

Felaco, M ;

Balbone, A ;

Angelucci, D ;

Gallina, S ;

Calafiore, AM ;

De Caterina, R ;

Barsotti, A .

AMERICAN HEART JOURNAL, 2003, 146 (06) :1105-1111

[23] Bax-induced caspase activation and apoptosis via cytochrome c release from mitochondria is inhibitable by Bcl-xL [J].

Finucane, DM ;

Bossy-Wetzel, E ;

Waterhouse, NJ ;

Cotter, TG ;

Green, DR .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (04) :2225-2233

[24] The role of dynamin-related protein 1, a mediator of mitochondrial fission, in apoptosis [J].

Frank, S ;

Gaume, B ;

Bergmann-Leitner, ES ;

Leitner, WW ;

Robert, EG ;

Catez, F ;

Smith, CL ;

Youle, RJ .

DEVELOPMENTAL CELL, 2001, 1 (04) :515-525

[25]

Gajkowska B, 2004, J MOL HISTOL, V35, P11

[26] Distinct pathways regulate proapoptotic Nix and BNip3 in cardiac stress [J].

Gálvez, AS ;

Brunskill, EW ;

Marreez, Y ;

Benner, BJ ;

Regula, KM ;

Kirschenbaum, LA ;

Dorn, GW .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (03) :1442-1448

[27] Endoplasmic reticulum BIK initiates DRP1-regulated remodelling of mitochondrial cristae during apoptosis [J].

Germain, M ;

Mathai, JP ;

McBride, HM ;

Shore, GC .

EMBO JOURNAL, 2005, 24 (08) :1546-1556

[28] The imbalance between Bim and Mcl-1 expression controls the survival of human myeloma cells [J].

Gomez-Bougie, P ;

Bataille, R ;

Amiot, M .

EUROPEAN JOURNAL OF IMMUNOLOGY, 2004, 34 (11) :3156-3164

[29] REPERFUSION INJURY INDUCES APOPTOSIS IN RABBIT CARDIOMYOCYTES [J].

GOTTLIEB, RA ;

BURLESON, KO ;

KLONER, RA ;

BABIOR, BM ;

ENGLER, RL .

JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (04) :1621-1628

[30] A unique pathway of cardiac myocyte death caused by hypoxia-acidosis [J].

Graham, RA ;

Frazier, DP ;

Thompson, JW ;

Haliko, S ;

Li, HF ;

Wasserlauf, BJ ;

Spiga, MG ;

Bishopric, NH ;

Webster, KA .

JOURNAL OF EXPERIMENTAL BIOLOGY, 2004, 207 (18) :3189-3200

← 1 2 3 4 5 6 7 8 9 10 →